PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31905343-6 2020 The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway. Cisplatin 38-47 BCL2 associated X, apoptosis regulator Homo sapiens 188-191 31807162-12 2019 In addition, combination of radiation and cisplatin had a higher inhibitory effect on Bax protein level and a higher inductive effect on Bcl-2 protein level compared with treatments with radiation and cisplatin alone. Cisplatin 42-51 BCL2 associated X, apoptosis regulator Homo sapiens 86-89 31541355-8 2019 Cisplatin + compound 4 significantly enhanced p53 phosphorylation, induced Bax amount, reduced Bcl2 protein levels, enhanced PARP cleavage and modulated miRNAs expression profile in TNBCs, with a particular overexpression of miR-125a-5p and miR-181a-5p. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 75-78 31699970-6 2019 Mitochondria are in two ways pivotal for cisplatin sensitivity because not only knock-down of BAX and BAK but also the ROS scavenger glutathione diminish cisplatin induced apoptosis. Cisplatin 41-50 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 32021975-9 2020 The cisplatin-induced apoptosis in endometrial cancer cells was inhibited by miR-135a by regulation of BAX and Bcl-2 expression. Cisplatin 4-13 BCL2 associated X, apoptosis regulator Homo sapiens 103-106 31609766-5 2019 SIN and cisplatin further decreased the Bcl-2, procaspase-3, and beta-catenin, but increased Bax, cleaved dcaspase 3, MMP9, and MMP2 in combined group than in either alone group. Cisplatin 8-17 BCL2 associated X, apoptosis regulator Homo sapiens 93-96 31411791-11 2019 Moreover, SKOV3/DDP cells had a lower miR-1271 level, and enhancing miR-1271 contributed strongly to cisplatin-induced apoptosis through altering the expressions of B-cell lymphoma-2 associated X protein (BAX), cleaved caspase-3 and B-cell lymphoma 2 (Bcl-2). Cisplatin 101-110 BCL2 associated X, apoptosis regulator Homo sapiens 205-208 31380278-7 2019 After cisplatin treatment, J cybrids showed increased gene expression of BAX, CASP3, and CYP51A, but lower levels of SFRP1 compared to untreated-J cybrids. Cisplatin 6-15 BCL2 associated X, apoptosis regulator Homo sapiens 73-76 31079851-11 2019 Moreover, apatinib increased cisplatin-induced apoptosis on MDA-MB-231 cells via increasing the level of Bax and active caspase 3 and decreasing the expression of Bcl-2. Cisplatin 29-38 BCL2 associated X, apoptosis regulator Homo sapiens 105-108 31173289-2 2019 PATIENTS AND METHODS: We detected the expressions of SNHG5, apoptosis-specific genes (Bax and Bcl-2) and drug resistance-specific genes (MDR1 and MRP1) in cisplatin-sensitive and cisplatin-resistant GC patients. Cisplatin 155-164 BCL2 associated X, apoptosis regulator Homo sapiens 86-89 30548903-6 2019 Screening of 6246 Generally Recognized As Safe compounds from four chemical libraries post-induction of cisplatin-mediated PCD resulted in the identification of 18 compounds which significantly reduced levels of Bax translocation. Cisplatin 104-113 BCL2 associated X, apoptosis regulator Homo sapiens 212-215 31010222-9 2019 Cisplatin increased the expression of Bax and reduced the expression of Bcl-2, which activate and inhibit, respectively, the mitochondrial apoptotic pathway in response to oxidative stress. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 38-41 30548903-8 2019 Consistent with their effects on Bax translocation, these compounds exhibited significant rescue against in vitro and in vivo cisplatin-induced apoptosis. Cisplatin 126-135 BCL2 associated X, apoptosis regulator Homo sapiens 33-36 30747218-5 2019 Notably, the results also indicated that GA enhanced the anticancer effects of cisplatin in the inhibition of cancer cell proliferation and the induction of cell apoptosis following elevated Bax expression and suppressed Bcl-2 expression. Cisplatin 79-88 BCL2 associated X, apoptosis regulator Homo sapiens 191-194 30923410-9 2019 Apoptotic cells, but not necrotic cells, were significantly increased following the combined treatment, and an increase in the Bax/Bcl-2 ratio indicated that the combination of cisplatin and SAHA induced apoptosis through the mitochondrial pathway. Cisplatin 177-186 BCL2 associated X, apoptosis regulator Homo sapiens 127-130 30503360-5 2019 Here, we found that the combination treatment of scutellarin and cisplatin enhanced apoptosis in ovarian cancer cells via increasing the extent of platinum-DNA adducts and the ratio of Bax/Bcl-2. Cisplatin 65-74 BCL2 associated X, apoptosis regulator Homo sapiens 185-188 30111297-12 2018 While cisplatin treatment decreased the ratio of Bcl-2 to Bax in normoxic condition, hypoxia conversely increased the ratio in HMM cells treated with cisplatin. Cisplatin 6-15 BCL2 associated X, apoptosis regulator Homo sapiens 58-61 30549344-3 2019 The status of Bax was analyzed at DNA/mRNA/protein levels and the results were correlated with p53 and Akt expression in tissue samples/cisplatin-resistant oral tongue SCC (SCC9/SCC4-CisR) cell line. Cisplatin 136-145 BCL2 associated X, apoptosis regulator Homo sapiens 14-17 30549344-7 2019 Akt Inhibitor VIII and nimbolide synergistically induce Bax, and it is therefore beneficial for chemosensitizing cisplatin-resistant human OSCC. Cisplatin 113-122 BCL2 associated X, apoptosis regulator Homo sapiens 56-59 30410558-4 2018 We found that the combined use of A549/DDP cells with SFI and cisplatin enhanced cell cycle arrested in the G2/M phase, which was accompanied by upregulation of p53 and p21 protein expression and induced mitochondrial apoptosis in conjunction with the upregulation of Bax and the downregulation of Bcl-2 protein expression. Cisplatin 62-71 BCL2 associated X, apoptosis regulator Homo sapiens 268-271 30008879-5 2018 Overexpression of miR-137 suppressed the protein expression of AKT2, increased caspase-3 activity, increased Bax protein expression and suppressed Cyclin D1 protein expression in A549 and H520 cells treated with cisplatin. Cisplatin 212-221 BCL2 associated X, apoptosis regulator Homo sapiens 109-112 30537795-9 2018 The survival rate and Bcl-2/Bax ratio of GIST-T1 cells treated with both Mir-22-3p analogue and cisplatin were significantly decreased, while the apoptosis rate and protein level of caspase-3 were significantly increased (p<0.05). Cisplatin 96-105 BCL2 associated X, apoptosis regulator Homo sapiens 28-31 30103745-4 2018 After treatment with 5 mug/mL cisplatin and 0.64 mg/mL SPS, the induction of apoptosis and the protein and mRNA expression of Bax, Bcl-2, COX-2, and cleaved caspase-3 in HN-6 cells were quantified. Cisplatin 30-39 BCL2 associated X, apoptosis regulator Homo sapiens 126-129 28692636-11 2017 Combination regimen could decrease expression of Bcl-2 and increase expression of Bax more than cisplatin or TQ alone. Cisplatin 96-105 BCL2 associated X, apoptosis regulator Homo sapiens 82-85 29548748-7 2018 MALAT1 knockdown enhanced CDDP-induced apoptosis in vivo, as indicated by upregulation of Bax protein expression and downregulation of Bcl-2 protein expression. Cisplatin 26-30 BCL2 associated X, apoptosis regulator Homo sapiens 90-93 29730910-13 2018 Furthermore, western blot results showed that the expression of Bax and caspase-3 protein was increased (P<0.05), whereas Bcl-2 and survivin was decreased (P<0.05) in the hGAG+ DDP group compared with cisplatin alone (P<0.05). Cisplatin 207-216 BCL2 associated X, apoptosis regulator Homo sapiens 64-67 29196192-7 2018 Moreover, macrovipecetin alone or combined with cisplatin induced the expression of TRADD, p53, Bax, Bim and Bad and down-regulated the Bcl-2 expression and ROS levels in SK-MEL-28 cells. Cisplatin 48-57 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 29434943-7 2018 All compounds used alone (Pt12, cisplatin and the anti-MUC1 antibody) increased the concentration of proapoptotic Bax, cytochrome c and caspase-9 in comparison with control, thus suggesting that they activated the mitochondrial apoptotic pathway. Cisplatin 32-41 BCL2 associated X, apoptosis regulator Homo sapiens 114-117 29091869-0 2018 Galangin (GG) combined with cisplatin (DDP) to suppress human lung cancer by inhibition of STAT3-regulated NF-kappaB and Bcl-2/Bax signaling pathways. Cisplatin 28-37 BCL2 associated X, apoptosis regulator Homo sapiens 127-130 28291626-7 2017 Mus81 knockdown also induced S phase arrest and elevated apoptosis in CDDP treated HCT116 cells through activating CHK1/CDC25A/CDK2 and CHK1/p53/Bax pathways, while these effects could be counteracted by CHK1 inhibition. Cisplatin 70-74 BCL2 associated X, apoptosis regulator Homo sapiens 145-148 29344640-6 2018 When EGFR protein expression was suppressed, PI3K, p-Akt, p-JAK2 and p-STAT3, decreased cyclin D1 and increased Bax protein expression in cisplatin-induced A549 cells by over-regulation of microRNA-133b. Cisplatin 138-147 BCL2 associated X, apoptosis regulator Homo sapiens 112-115 29254192-8 2017 Moreover, treating CCDC69 knockout A2780cis cells with cisplatin, abrogated G1 and G2/M arrest, increased of cleaved caspase 3&8, greater DeltaPsim loss and higher levels of Bax were observed. Cisplatin 55-64 BCL2 associated X, apoptosis regulator Homo sapiens 178-181 28979680-10 2017 After treatment of cisplatin, SKOV3 and hey cells showed increased apoptotic rate in flow cytometry assay, increased protein levels of cleaved caspase 3, cleaved PARP and Bax, and decreased protein levels of Bcl-2 and Bcl-XL. Cisplatin 19-28 BCL2 associated X, apoptosis regulator Homo sapiens 171-174 31966904-0 2017 miR-181 regulation of BAX controls cisplatin sensitivity of prostate cancer cells. Cisplatin 35-44 BCL2 associated X, apoptosis regulator Homo sapiens 22-25 28214344-5 2017 Furthermore our results revealed that neferine combined with cisplatin down regulate the expression of Bcl-2 and up regulate the expression of Bax, Bad, Bak, release of cytochrome c, p53 levels, then activated cleavage forms of caspase-9, caspase-3, and PARP. Cisplatin 61-70 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 31966904-9 2017 Mechanistically, we demonstrate the pro-apoptotic protein, BAX, is typically enhanced by cisplatin treatment but its suppression promoted resistance. Cisplatin 89-98 BCL2 associated X, apoptosis regulator Homo sapiens 59-62 31966904-11 2017 We subsequently show that BAX expression restored cisplatin sensitivity in miR-181a overexpressing prostate cancer cells. Cisplatin 50-59 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 27601167-16 2016 Finally, data suggest that GANT61 could enhance cisplatin-induced apoptosis through promoting the expression of Bax, caspase-3 and caspase-9 protein levels. Cisplatin 48-57 BCL2 associated X, apoptosis regulator Homo sapiens 112-115 29084683-8 2017 The treatment of crocin plus cisplatin significantly increased the expression of p53 and Bax (p< 0.05), and significantly decreased the Bcl-2 expression (p<0.05). Cisplatin 29-38 BCL2 associated X, apoptosis regulator Homo sapiens 89-92 28789701-7 2017 Ad5/F11p-PSCAE-UPII-E1A plus cisplatin could upregulate the proteins expression of p53, Bax, and cleaved caspase-3, and downregulated Bcl-2 protein expression in T24, EJ and 5637 cells. Cisplatin 29-38 BCL2 associated X, apoptosis regulator Homo sapiens 88-91 28567015-8 2017 In summary, our findings reveal the dual mechanism of USP22 involvement in cisplatin resistance that USP22 can regulate gammaH2AX-mediated DNA damage repair and Ku70/Bax-mediated apoptosis. Cisplatin 75-84 BCL2 associated X, apoptosis regulator Homo sapiens 166-169 28454469-10 2017 Baicalein and baicalein-cisplatin combination treatments also inhibited B cell lymphoma-2 (Bcl-2) and increased Bcl-2-associated X protein (Bax) expression. Cisplatin 24-33 BCL2 associated X, apoptosis regulator Homo sapiens 112-138 28454469-10 2017 Baicalein and baicalein-cisplatin combination treatments also inhibited B cell lymphoma-2 (Bcl-2) and increased Bcl-2-associated X protein (Bax) expression. Cisplatin 24-33 BCL2 associated X, apoptosis regulator Homo sapiens 140-143 28454469-13 2017 The present study concluded that baicalein combined with cisplatin induced cytotoxicity and apoptosis of A549 cells, and such activity may be associated with the regulation of Bcl-2, Bax and caspase-3, indicating a promising alternative method for lung cancer. Cisplatin 57-66 BCL2 associated X, apoptosis regulator Homo sapiens 183-186 28355175-8 2017 Cisplatin combined with beta-elemene decreased the expressions of p-STAT3, p-JAK2, and Bcl-2, and increased the expressions of Bax and caspase-3 significantly compared to cisplatin only treatment, as well as in the xenograft model. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 127-130 28386348-5 2017 Firstly, we found cisplatin induced cell apoptosis in mesangial cells shown by increased number of apoptotic cells in parallel with the upregulation of Bax and the downregulation of Bcl-2. Cisplatin 18-27 BCL2 associated X, apoptosis regulator Homo sapiens 152-155 28386348-7 2017 Importantly, inhibition of COX-2 via a specific COX-2 inhibitor celecoxib markedly blocked cisplatin-induced mesangial cell apoptosis as evidenced by the decreased number of apoptotic cells, blocked increments of cleaved caspase-3 and Bax, and reversed Bcl-2 downregulation. Cisplatin 91-100 BCL2 associated X, apoptosis regulator Homo sapiens 235-238 28056551-11 2017 Hepatitis B X-interacting protein and cisplatin cooperated to induce apoptosis and increase the expression of c-caspase 3 as well as the Bax/Bcl-2 ratio. Cisplatin 38-47 BCL2 associated X, apoptosis regulator Homo sapiens 137-140 28471109-8 2017 In addition, cisplatin increased the ratio of Bax to Bcl-2 in K562, which can influence the mitochondrial membrane permeability. Cisplatin 13-22 BCL2 associated X, apoptosis regulator Homo sapiens 46-49 28124680-9 2017 The level of Bcl-2 decreased, while the levels of Bax, caspase-3, and caspase-9 increased in cisplatin combined with APS treatment compared to cisplatin only treatment. Cisplatin 93-102 BCL2 associated X, apoptosis regulator Homo sapiens 50-53 28124680-10 2017 The ratio of Bax to Bcl-2 was significantly enhanced by the APS to cisplatin. Cisplatin 67-76 BCL2 associated X, apoptosis regulator Homo sapiens 13-16 28124680-11 2017 CONCLUSIONS APS enhanced the anti-proliferative and apoptotic effect of cisplatin by modulating expression of Bax/Bcl-2 ratio and caspases on nasopharyngeal carcinoma cells and in the xenograft model. Cisplatin 72-81 BCL2 associated X, apoptosis regulator Homo sapiens 110-113 27806086-8 2016 Ptac2S was more efficacious than cisplatin also in inducing apoptosis characterized by: (a) mitochondria depolarization, (b) increase of bax expression and its cytosol-to-mitochondria translocation and decrease of Bcl-2 expression, (c) activation of caspase-7 and -9. Cisplatin 33-42 BCL2 associated X, apoptosis regulator Homo sapiens 137-140 27591926-4 2016 CDDP/RSV increased ROS production and depolarization of mitochondrial membrane potential with an increase in the Bax/Bcl-2 ratio. Cisplatin 0-4 BCL2 associated X, apoptosis regulator Homo sapiens 113-116 27825085-0 2016 AKT2 inhibition of cisplatin-induced JNK/p38 and Bax activation by phosphorylation of ASK1. Cisplatin 19-28 BCL2 associated X, apoptosis regulator Homo sapiens 49-52 27588477-9 2016 Furthermore, we found that the PI3K/AKT pathway and Bcl-2/Bax ratio might be responsible for the eIF4E-induced cisplatin resistance in ESCC. Cisplatin 111-120 BCL2 associated X, apoptosis regulator Homo sapiens 58-61 27484725-11 2016 This suggested that the enhanced cisplatin chemosensitivity with Ad-ING4-P53 gene therapy in hypopharyngeal cancer xenografts may be associated with apoptosis induction through upregulation of Bax expression and downregulation of Bcl-2. Cisplatin 33-42 BCL2 associated X, apoptosis regulator Homo sapiens 193-196 27494891-6 2016 Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP. Cisplatin 79-88 BCL2 associated X, apoptosis regulator Homo sapiens 282-285 27419628-5 2016 The results showed that both glutamine deprivation and BPTES pretreatments increased the toxic effects of cisplatin and etoposide on HCC1937 cells, as demonstrated by their reduced proliferation, increased expression of apoptosis-related proteins (cleaved-PARP, cleaved-caspase 9, and cleaved-caspase 3) and decreased Bcl-2/BAX ratio. Cisplatin 106-115 BCL2 associated X, apoptosis regulator Homo sapiens 324-327 27129294-9 2016 Exogenous STAT3 and CDDP may synergistically inhibit the xenograft tumour growth through up-regulation of BAX protein via GRP78. Cisplatin 20-24 BCL2 associated X, apoptosis regulator Homo sapiens 106-109 27484725-10 2016 The results of immunohistochemistry analysis demonstrated that Bax expression was increased and Bcl-2 was decreased in the Ad-ING4-P53 + cisplatin group. Cisplatin 137-146 BCL2 associated X, apoptosis regulator Homo sapiens 63-66 29714913-1 2016 Lung cancer is the leading cause of cancer-related deaths worldwide.Despite the development and use of several targeting drugs for lung cancer therapy,the five-year survival rate has remained as low as 15%for the past three decades.Cisplatin-based chemotherapy is considered the first-line therapeutic strategy for lung cancer.However,developments of chemoresistance is a major obstacle for the successful treatment.Therefore,the development of novel therapy against cisplatin-resistance lung cancer is imperative.Photodynamic therapy(PDT),which is a non-invasive combinatorial therapeutic modality using light,photosensitizer(PS)and oxygen,may provide an unprecedented tool to develop more effective treatments.To provide experimental basis for its application in cisplatin-resistance lung cancer,we will discuss the biological effects of MPPa-photodynamic therapy in human cisplatin-resistance lung cancer cells in this article.Human cisplatin-resistance lung cancer cells A549/DDP were co-cultured with MPPa(0,1,2,4,8,16mumol/L)and exposed to light(0,0.6,1.2,2.4,3.6,4.8J/cm2),and cell viability was determined with CCK-8assay.Flow cytometry was used to detect apoptosis,DCFH-DA staining was employed to observe reactive oxygen species(ROS),and Western blot was used to detect the expressions of B-cell lymphoma-2(Bcl-2)protein and Bcl-2associated X protein(Bax).The proliferation of A549/DDP cells was suppressed by PDT.The apoptotic rate in the PDT group was significantly higher than that in the control,MPPa or light group(P<0.05).The level of ROS was increased.The expression of Bax was increased,and that of Bcl-2was decreased.MPPa-photodynamic therapy can significantly suppress cell viability,and induce apoptosis in human cisplatin-resistance lung cancer cells. Cisplatin 232-241 BCL2 associated X, apoptosis regulator Homo sapiens 1361-1364 29714913-1 2016 Lung cancer is the leading cause of cancer-related deaths worldwide.Despite the development and use of several targeting drugs for lung cancer therapy,the five-year survival rate has remained as low as 15%for the past three decades.Cisplatin-based chemotherapy is considered the first-line therapeutic strategy for lung cancer.However,developments of chemoresistance is a major obstacle for the successful treatment.Therefore,the development of novel therapy against cisplatin-resistance lung cancer is imperative.Photodynamic therapy(PDT),which is a non-invasive combinatorial therapeutic modality using light,photosensitizer(PS)and oxygen,may provide an unprecedented tool to develop more effective treatments.To provide experimental basis for its application in cisplatin-resistance lung cancer,we will discuss the biological effects of MPPa-photodynamic therapy in human cisplatin-resistance lung cancer cells in this article.Human cisplatin-resistance lung cancer cells A549/DDP were co-cultured with MPPa(0,1,2,4,8,16mumol/L)and exposed to light(0,0.6,1.2,2.4,3.6,4.8J/cm2),and cell viability was determined with CCK-8assay.Flow cytometry was used to detect apoptosis,DCFH-DA staining was employed to observe reactive oxygen species(ROS),and Western blot was used to detect the expressions of B-cell lymphoma-2(Bcl-2)protein and Bcl-2associated X protein(Bax).The proliferation of A549/DDP cells was suppressed by PDT.The apoptotic rate in the PDT group was significantly higher than that in the control,MPPa or light group(P<0.05).The level of ROS was increased.The expression of Bax was increased,and that of Bcl-2was decreased.MPPa-photodynamic therapy can significantly suppress cell viability,and induce apoptosis in human cisplatin-resistance lung cancer cells. Cisplatin 232-241 BCL2 associated X, apoptosis regulator Homo sapiens 1590-1593 26984736-2 2016 In Cisplatin-sensitive cells Cisplatin treatment increases p53-protein level as well as downstream signaling, e.g., expression of p21(Waf1/Cip1), Bax, Noxa, MDM2, and activation of Caspase-9/-3. Cisplatin 3-12 BCL2 associated X, apoptosis regulator Homo sapiens 146-149 26987028-10 2016 The results showed that both GA and cisplatin changed the morphology, inhibited the growth and induced apoptosis in the H446 cells by inducing generation of ROS, disruption of MMP, downregulation of XIAP expression, and upregulation of Bax, Apaf-1, DIABLO and p53 expression. Cisplatin 36-45 BCL2 associated X, apoptosis regulator Homo sapiens 236-239 26984736-2 2016 In Cisplatin-sensitive cells Cisplatin treatment increases p53-protein level as well as downstream signaling, e.g., expression of p21(Waf1/Cip1), Bax, Noxa, MDM2, and activation of Caspase-9/-3. Cisplatin 29-38 BCL2 associated X, apoptosis regulator Homo sapiens 146-149 26996126-0 2016 Cisplatin-induced apoptosis in non-small-cell lung cancer cells is dependent on Bax- and Bak-induction pathway and synergistically activated by BH3-mimetic ABT-263 in p53 wild-type and mutant cells. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 80-83 26996126-4 2016 In contrast, the expression of proapoptotic multidomain Bcl-2-family members, Bak and Bax, was induced by cisplatin in p53-dependent and -independent manners, respectively. Cisplatin 106-115 BCL2 associated X, apoptosis regulator Homo sapiens 86-89 26996126-5 2016 Moreover, in wild-type p53-expressing cells, cisplatin mainly used the Bak-dependent apoptotic pathway, but this apoptotic pathway shifted to the Bax-dependent pathway by loss-of-function of p53. Cisplatin 45-54 BCL2 associated X, apoptosis regulator Homo sapiens 146-149 27029054-6 2016 Furthermore, Exo-GF co-incubation with cisplatin increased autophagic activity and reduced apoptosis, as demonstrated by an upregulation of LC3-II and Bcl-2 protein levels and downregulation of p62 and Bax protein levels. Cisplatin 39-48 BCL2 associated X, apoptosis regulator Homo sapiens 202-205 26356820-10 2015 Bax-PGAM5L-Drp1 complex is detected in arenobufagin and staurosporine treated CRC cells in vitro and in arenobufagin and cisplatin treated tumor in vivo as well. Cisplatin 121-130 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 26503209-0 2016 Knockdown of miR-221 promotes the cisplatin-inducing apoptosis by targeting the BIM-Bax/Bak axis in breast cancer. Cisplatin 34-43 BCL2 associated X, apoptosis regulator Homo sapiens 84-87 26503209-8 2016 Our results suggest the anti-miR-221 could promote the cisplatin-inducing apoptosis by targeting the Bim-Bax/Bak axis in breast cancer. Cisplatin 55-64 BCL2 associated X, apoptosis regulator Homo sapiens 105-108 26729257-4 2016 We showed that a pretreatment with morphine (1 mug/ml) inhibited the sensitivity of CNE-2 cells to cisplatin by inhibiting cisplatin-induced CNE-2 cell apoptosis, decreasing caspase-3 activity and increasing the Bcl-2/Bax ratio. Cisplatin 99-108 BCL2 associated X, apoptosis regulator Homo sapiens 218-221 26925782-6 2016 The present study also demonstrated that hyperactivation of PI3K/Aktpathway is closely associated with cisplatin resistance by regulating the Bax-mitochondria-mediated apoptosis pathway in human lung cancer. Cisplatin 103-112 BCL2 associated X, apoptosis regulator Homo sapiens 142-145 26925782-7 2016 Inhibition of PI3K/Aktactivity in A549/DDP cells and H460/DDP cells could reverse cisplatin resistance by enhancing the effect of cisplatin on Bax oligomerization and release of Cytochrome C, allowing activation of the caspase-mediated apoptosis pathway. Cisplatin 130-139 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 26549524-8 2016 A549 cells exposed to the chemotherapeutic drug cisplatin (10 muM, 24 h) reveal signs of apoptosis, i.e. 25% reduction in cell viability as well as 1.3-, 1.5- and 3.3-fold increase in the expression of LRRC8A, Bax (regulator of apoptosis) and p21 (regulator of cell cycle progression), respectively. Cisplatin 48-57 BCL2 associated X, apoptosis regulator Homo sapiens 210-213 26314326-5 2015 Above all, resveratrol enhanced the effects of cisplatin on inhibition of cancer cell proliferation, induction of cell apoptosis, depolarization of mitochondrial membrane potential, release of cytochrome c and regulation on expression of Bcl-2 and Bax. Cisplatin 47-56 BCL2 associated X, apoptosis regulator Homo sapiens 248-251 26310353-14 2015 FoxO3a target genes involved in cell cycle progression and apoptosis were also investigated, and combined treatment with butein and cisplatin resulted in the downregulation of cyclin D1 and Bcl-2 and the upregulation of p27 and Bax. Cisplatin 132-141 BCL2 associated X, apoptosis regulator Homo sapiens 228-231 25770930-4 2015 Combination of chrysin and cisplatin increased the phosphorylation and accumulation of p53 through activating ERK1/2 in Hep G2 cells, which led to the overexpression of the pro-apoptotic proteins Bax and DR5 and the inhibition of the anti-apoptotic protein Bcl-2. Cisplatin 27-36 BCL2 associated X, apoptosis regulator Homo sapiens 196-199 25695150-5 2015 The mRNA expression levels of p53, p53beta and B-cell lymphoma 2-associated X protein (Bax) were detected in the MKN45 and SGC-7901 cells following treatment with cisplatin by reverse transcription-PCR. Cisplatin 163-172 BCL2 associated X, apoptosis regulator Homo sapiens 47-85 25695150-5 2015 The mRNA expression levels of p53, p53beta and B-cell lymphoma 2-associated X protein (Bax) were detected in the MKN45 and SGC-7901 cells following treatment with cisplatin by reverse transcription-PCR. Cisplatin 163-172 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 25695150-10 2015 In the MKN45 cells, p53beta, p53 and Bax mRNA expression levels gradually increased with the dose of cisplatin, and the expression of p53beta was positively correlated with the expression of p53 (tr=6.358, P<0.05) and Bax (tr=8.023, P<0.05). Cisplatin 101-110 BCL2 associated X, apoptosis regulator Homo sapiens 37-40 26403741-6 2015 The STOML-2-overexpressing cells exhibited an obvious resistance to IC50 Cisplatin-induced apoptosis as shown by both fluorescence microscopy and flow cytometry and presented with decreased expressions of cleaved caspase-3, Bax, and cytosol Cyt C and increased expressions of caspase-3, Bcl-2, and mitochondrial Cyt C. Cisplatin 73-82 BCL2 associated X, apoptosis regulator Homo sapiens 224-227 26366416-6 2015 Our study found that cisplatin induced apoptosis of Hela cell through inhibiting expression of Bcl-2, upregulating the expression of Bax, Fas-L, and the enzyme activity of caspase-3 (p < 0.05); LPA significantly provided protection against the apoptosis induced by cisplatin by inhibiting the above alterations in apoptotic factor caused by cisplatin (p < 0.05). Cisplatin 21-30 BCL2 associated X, apoptosis regulator Homo sapiens 133-136 25695283-9 2015 Overexpression of LRIG1 increased the inhibitory effect of CDDP on the T24 cell line, which may be associated with inactivation of the EGFR signaling pathway, followed by the decrease of Bcl-2 expression and a concomitantly induced expression of Bax. Cisplatin 59-63 BCL2 associated X, apoptosis regulator Homo sapiens 246-249 25582599-2 2015 The proapoptotic Bcl-2 family proteins Bax and Bak are essential for cisplatin-induced apoptosis. Cisplatin 69-78 BCL2 associated X, apoptosis regulator Homo sapiens 39-42 25092426-5 2014 Following treatment with cisplatin, the protein expression of GPR40 in the kidneys was decreased in association with an increase in serum creatinine levels and the Bax/Bcl-2 expression ratio. Cisplatin 25-34 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 26645893-8 2015 Finally, melatonin was able to strengthen cisplatin-mediated antitumour effects in human gastric carcinoma cells by up-regulating the expression of Bax, down-regulating the expression of Bcl-2 and activating the caspase-dependent apoptotic pathway. Cisplatin 42-51 BCL2 associated X, apoptosis regulator Homo sapiens 148-151 25613618-5 2015 ERbeta overexpression significantly reduced while ERbeta knockdown increased Bax activation and cell apoptosis induced by cisplatin and STS. Cisplatin 122-131 BCL2 associated X, apoptosis regulator Homo sapiens 77-80 24990093-7 2014 Cisplatin and [Pt(O,O"-acac)(gamma-acac)(DMS)] caused activation of caspases, proteolysis of PARP and modulation of Bcl-2, Bax and Bid. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 123-126 25289046-9 2014 Thus, ECRG2 in combination with DDP had an enhanced inhibitory effect on EC9706 cell proliferation compared with that of ECRG2 alone, and an increased inductive effect on EC9706 cell apoptosis, possibly due to the upregulation of the expression of Bax. Cisplatin 32-35 BCL2 associated X, apoptosis regulator Homo sapiens 248-251 25092426-10 2014 Treatment with cisplatin increased the Bax/Bcl-2 expression ratio and cleaved caspase-3 expression, and promoted the activation of nuclear factor-kappaB (NF-kappaB). Cisplatin 15-24 BCL2 associated X, apoptosis regulator Homo sapiens 39-42 24824514-9 2014 Moreover, the ability of doxorubicin, SN-38 and CDDP to induce proapoptotic signals was weaker in Rho cells, as evidenced by survivin upregulation and reductions in Bax/Bcl-2 expression ratios. Cisplatin 48-52 BCL2 associated X, apoptosis regulator Homo sapiens 165-168 24829158-4 2014 CDDP induced apoptosis within cells through the generation of reactive oxygen species (ROS), regulated the ROS-mediated expression of Bax, Bcl-2, and p53, and induced the degradation of the poly (ADP-ribosyl) polymerase (PARP). Cisplatin 0-4 BCL2 associated X, apoptosis regulator Homo sapiens 134-137 24573222-14 2014 The results of this study suggest that 1,25(OH)2D3 potentiates cisplatin-mediated cell growth inhibition and cell apoptosis, which involves the upregulation of Bax, a decrease in ERK and AKT phosphorylation levels, and increased p21 and p27 levels. Cisplatin 63-72 BCL2 associated X, apoptosis regulator Homo sapiens 160-163 24799992-9 2014 Melatonin reduced cisplatin-induced cell death, decreasing phosphorylated p53 apoptotic protein, cleaved caspase 3 and Bax levels but increasing anti-apoptotic Bcl-2 gene and protein expression. Cisplatin 18-27 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 24563380-6 2014 The addition of Andro to CDDP induced synergistic apoptosis, which could be corroborated to the changes in protein and mRNA levels of Bax and Bcl-2, and the increased Fas/FasL association in these cells, resulting in increased release of cytochrome c, and activation of caspases. Cisplatin 25-29 BCL2 associated X, apoptosis regulator Homo sapiens 134-137 24563380-7 2014 Pretreatment of Nok-1 monoclonal antibody, a Fas signaling inhibitor, or Bax inhibitor peptide V5 repressed the Andro-induced cleavage of procaspase and the sensitization to CDDP-induced apoptosis. Cisplatin 174-178 BCL2 associated X, apoptosis regulator Homo sapiens 73-76 24366574-8 2014 These findings, together with significantly elevated MT, decreased p53 and Bax indicate PC-3 to be cisplatin-resistant. Cisplatin 99-108 BCL2 associated X, apoptosis regulator Homo sapiens 75-78 24362790-4 2014 Our results indicate that the RasGAP-derived peptide increases cisplatin-induced Bax activation. Cisplatin 63-72 BCL2 associated X, apoptosis regulator Homo sapiens 81-84 24323562-0 2014 p21 overexpression sensitizes osteosarcoma U2OS cells to cisplatin via evoking caspase-3 and Bax/Bcl-2 cascade. Cisplatin 57-66 BCL2 associated X, apoptosis regulator Homo sapiens 93-96 24323562-7 2014 However, U2O3-p21 cells underwent more obvious apoptotic morphological changes than U2OS and U2OS-vec cells after being treated with cisplatin (5 mug) for 72 h. Besides, increased expression of cleaved caspase-3 and Bax/Bcl-2 ratio was observed in cisplatin-treated U2O3-p21 cells. Cisplatin 133-142 BCL2 associated X, apoptosis regulator Homo sapiens 216-219 24323562-8 2014 These data clearly indicated that exogenous p21 gene transfection could enhance the cisplatin-induced cytotoxicity against human osteosarcoma U2OS cells, at least in part, by activating caspase-3 cascade and increasing Bax/Bcl-2 ratio. Cisplatin 84-93 BCL2 associated X, apoptosis regulator Homo sapiens 219-222 24215867-4 2014 Here we show that p38alpha pharmacological inhibition combined with cisplatin administration decreases colony formation and viability of cancer cells and strongly increases Bax-dependent apoptotic cell death by activating the tumor suppressor protein FoxO3A. Cisplatin 68-77 BCL2 associated X, apoptosis regulator Homo sapiens 173-176 24854102-2 2014 When compared with a blank control group, the proportion of apoptotic cells undergoing Beclin 1 interfering increased significantly after cisplatin treatment, accompanied by reduction in mitochondrial membrane potential, increase in activities of caspase-9/3 and cytoplasmic cytochrome C, elevation of Bax expression, and reduction in Bcl-2 expression. Cisplatin 138-147 BCL2 associated X, apoptosis regulator Homo sapiens 302-305 24507386-14 2014 The tumor tissues were harvested after treatment, and ACBP-L and Cisplatin treatment suppressed Bcl-2, and induced Bax, Caspase 3, and Caspase 8 molecules as detected by RT-PCR and immunohistochemistry. Cisplatin 65-74 BCL2 associated X, apoptosis regulator Homo sapiens 115-118 23970333-0 2013 p53 restoration can overcome cisplatin resistance through inhibition of Akt as well as induction of Bax. Cisplatin 29-38 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 23970333-7 2013 In addition, the ratio of Bax to Bcl-2 was increased by CDDP treatment in SNU-1 cells, but not in SNU-16 cells. Cisplatin 56-60 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 23970333-12 2013 The induction of wild-type p53 can enhance CDDP-induced apoptosis not only by inducing Bax protein but also by suppressing anti-apoptotic proteins through inhibition of Akt. Cisplatin 43-47 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 24084596-9 2013 With cisplatin treatment, the expression of phosphorylated PERK and eIF-2alpha, CCAAT/enhancer-binding protein-homologous protein, Bax, and caspase-4 and -7 was higher and the cell viability was lower (P < .01) in FL-RECK-overexpressing cells than in del-C-RECK-overexpressing or vector control cells. Cisplatin 5-14 BCL2 associated X, apoptosis regulator Homo sapiens 131-134 23665025-8 2013 We found that the combination of cisplatin and STAT3 siRNA resulted in the collapse of the mitochondrial membrane potential, attenuated the expression of Bcl-xL and Bcl-2, and increased the release of cytochrome C and expression of Bax. Cisplatin 33-42 BCL2 associated X, apoptosis regulator Homo sapiens 232-235 23485394-7 2013 In addition, although Bax deficiency rendered cells resistant to PU-H71, combined treatment with the anticancer drugs cisplatin or melphalan greatly sensitized these cells to PU-H71. Cisplatin 118-127 BCL2 associated X, apoptosis regulator Homo sapiens 22-25 23826494-0 2013 Synergistic Effect of Subtoxic-dose Cisplatin and TRAIL to Mediate Apoptosis by Down-regulating Decoy Receptor 2 and Up-regulating Caspase-8, Caspase-9 and Bax Expression on NCI-H460 and A549 Cells. Cisplatin 36-45 BCL2 associated X, apoptosis regulator Homo sapiens 156-159 23076534-6 2013 Periostin-overexpressing cells treated with cisplatin or 5-FU showed significantly (p < 0.05) decreased expression of Bax and p53 proteins and increased expression of Bcl-2 protein, when compared to drug-treated mock counterparts. Cisplatin 44-53 BCL2 associated X, apoptosis regulator Homo sapiens 121-124 23188704-5 2013 From among a panel of apoptosis-related factors (p53, Bcl-2, Bcl-XL, BAX, and survivin), the expression of Livin was upregulated after cisplatin treatment in a dose-dependent manner. Cisplatin 135-144 BCL2 associated X, apoptosis regulator Homo sapiens 69-72 24001324-9 2013 Activated caspase 3 and Bax/Bcl-2 ratio were significantly increased in Cisplatin-treated cells. Cisplatin 72-81 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 23533654-9 2013 In combination with NVP-BEZ235 and CDDP, there was dramatic synergy in shrinking tumor volumes and inducing apoptosis through increasing Noxa, Bax and decreasing Mcl-1, Bcl-2. Cisplatin 35-39 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 23254292-3 2012 Here, we show that cisplatin can efficiently bypass mitochondrial apoptosis block caused by loss of BAX and BAK, via activation of the extrinsic death receptor pathway in some model cell lines. Cisplatin 19-28 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 22340096-10 2011 Compared with the single use of cisplatin, the combination of ABT-737 and cisplatin accelerated the cleavage of PARP and caspase3, but did not alter the expression levels of Bcl-2, Bcl-X(L), and Bax. Cisplatin 74-83 BCL2 associated X, apoptosis regulator Homo sapiens 195-198 23437261-11 2013 CONCLUSIONS: BH3-mimetic ABT737 not only requires Bax/Bak to exert its apoptosis-inducing effect, but also Apaf-1, while GX15-070 and CDDP induce different modalities of cell death in the absence of Bax/Bak or Apaf-1. Cisplatin 134-138 BCL2 associated X, apoptosis regulator Homo sapiens 199-202 22281241-3 2012 Bax translocation to mitochondria is required for mitochondrial protein release and cisplatin-induced apoptosis in human ovarian cancer cells. Cisplatin 84-93 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 22562580-7 2012 In addition, siRNA against NOX3 reduced apoptosis as demonstrated by TUNEL staining, and prevented the increased expression of Bax and abrogated the decrease in Bcl2 expression following cisplatin administration. Cisplatin 187-196 BCL2 associated X, apoptosis regulator Homo sapiens 127-130 22699051-9 2012 Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3. Cisplatin 30-39 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 22238053-0 2012 Quantitative expression analysis of the apoptosis-related genes BCL2, BAX and BCL2L12 in gastric adenocarcinoma cells following treatment with the anticancer drugs cisplatin, etoposide and taxol. Cisplatin 164-173 BCL2 associated X, apoptosis regulator Homo sapiens 70-73 22238053-11 2012 Treatment of AGS cells with 10 muM cisplatin, 0.5 muM etoposide and 10 nM taxol affected the BCL2, BAX and BCL2L12 mRNA levels, compared to the untreated cells. Cisplatin 35-44 BCL2 associated X, apoptosis regulator Homo sapiens 99-102 22020779-8 2012 Silencing HERG inhibited the apoptosis induced by cisplatin both in vitro and in vivo, by attenuating the cisplatin effects on Bcl-2, Bax and active caspase-3. Cisplatin 62-71 BCL2 associated X, apoptosis regulator Homo sapiens 158-161 22020779-8 2012 Silencing HERG inhibited the apoptosis induced by cisplatin both in vitro and in vivo, by attenuating the cisplatin effects on Bcl-2, Bax and active caspase-3. Cisplatin 118-127 BCL2 associated X, apoptosis regulator Homo sapiens 158-161 22052903-14 2012 Therefore, Smac mediates Bax activation to determine the threshold for overcoming cisplatin resistance in ovarian cancer cells. Cisplatin 82-91 BCL2 associated X, apoptosis regulator Homo sapiens 25-28 22524836-9 2012 The increased apoptotic sensitivity of SGC7901/ DDP to cisplatin was due to the decreasing proportion of Bcl-2/Bax via down-regulating NF-kB. Cisplatin 55-64 BCL2 associated X, apoptosis regulator Homo sapiens 111-114 22590594-0 2012 NOXA-induced alterations in the Bax/Smac axis enhance sensitivity of ovarian cancer cells to cisplatin. Cisplatin 93-102 BCL2 associated X, apoptosis regulator Homo sapiens 32-35 22590594-4 2012 In this study, we found that genetic variants of Bcl-2 proteins exist among cisplatin-sensitive and -resistant ovarian cancer cells, and the responses of NOXA and Bax to cisplatin are regulated mainly by p53. Cisplatin 170-179 BCL2 associated X, apoptosis regulator Homo sapiens 163-166 22590594-8 2012 Furthermore, gene silencing of Bax or Smac significantly attenuated NOXA and/or cisplatin-induced apoptosis in chemosensitive A2780s cells, whereas overexpression of Bax or addition of Smac-N7 peptide significantly increased NOXA and/or cisplatin-induced apoptosis in chemoresistant SKOV3 cells. Cisplatin 80-89 BCL2 associated X, apoptosis regulator Homo sapiens 31-34 22590594-8 2012 Furthermore, gene silencing of Bax or Smac significantly attenuated NOXA and/or cisplatin-induced apoptosis in chemosensitive A2780s cells, whereas overexpression of Bax or addition of Smac-N7 peptide significantly increased NOXA and/or cisplatin-induced apoptosis in chemoresistant SKOV3 cells. Cisplatin 237-246 BCL2 associated X, apoptosis regulator Homo sapiens 31-34 22590594-9 2012 To our knowledge, these data suggest a new mechanism by which NOXA chemosensitized ovarian cancer cells to cisplatin by inducing alterations in the Bax/Smac axis. Cisplatin 107-116 BCL2 associated X, apoptosis regulator Homo sapiens 148-151 22349377-9 2012 The expression of C23, Bcl-2 mRNA and protein was weaker and that of Bax mRNA and protein was stronger in the AS+DDP group compared with the DDP group (P<0.01). Cisplatin 113-116 BCL2 associated X, apoptosis regulator Homo sapiens 69-72 25045421-8 2012 Expressions of pro-apoptotic factors (cleaved caspase-3/-8/-9 and bax) were increased by the combinational treatment with PQ1 and cisplatin; whereas, the pro-survival factor, bcl-2, was decreased by the combinational treatment. Cisplatin 130-139 BCL2 associated X, apoptosis regulator Homo sapiens 66-69 22445428-3 2012 Here we show that cisplatin induced several platelet apoptotic events including up-regulation of Bax and Bak, down-regulation of Bcl-2 and Bcl-X(L), mitochondrial translocation of Bax, mitochondrial inner transmembrane potential depolarization, caspase-3 activation and phosphatidylserine (PS) exposure. Cisplatin 18-27 BCL2 associated X, apoptosis regulator Homo sapiens 97-100 22445428-3 2012 Here we show that cisplatin induced several platelet apoptotic events including up-regulation of Bax and Bak, down-regulation of Bcl-2 and Bcl-X(L), mitochondrial translocation of Bax, mitochondrial inner transmembrane potential depolarization, caspase-3 activation and phosphatidylserine (PS) exposure. Cisplatin 18-27 BCL2 associated X, apoptosis regulator Homo sapiens 180-183 22056880-5 2012 In addition, Bax deficiency only provides partial protection against camptothecin and cisplatin-induced apoptosis and no protection against killing by Puma or ABT-737 plus Noxa overexpression. Cisplatin 86-95 BCL2 associated X, apoptosis regulator Homo sapiens 13-16 21935568-0 2011 The potent peptide antagonist to angiogenesis, C16Y, and cisplatin act synergistically in the down-regulation of the Bcl-2/Bax ratio and the induction of apoptosis in human ovarian cancer cells. Cisplatin 57-66 BCL2 associated X, apoptosis regulator Homo sapiens 123-126 21935568-11 2011 These observations suggest that the suppression of the Bcl-2/Bax ratio may play an important role in mediating the synergistic effect of cisplatin and C16Y on the induction of apoptosis in OVACAR3 cells. Cisplatin 137-146 BCL2 associated X, apoptosis regulator Homo sapiens 61-64 21953469-5 2011 As a consequence, cells expressing p53 K351N mutant showed defects in cisplatin-induced translocation of p53 to mitochondria, Bax oligomerization, and mitochondrial membrane depolarization. Cisplatin 70-79 BCL2 associated X, apoptosis regulator Homo sapiens 126-129 21660965-9 2011 Notably, the effects of CITED2 knockdown on p53 accumulation and the increase of p53"s target Bax were more pronounced after treatment with cisplatin. Cisplatin 140-149 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 21145397-3 2011 We have previously shown that cisplatin induces apoptosis in dorsal root ganglion (DRG) sensory neurons by covalently binding to nuclear DNA (nDNA), resulting in DNA damage, subsequent p53 activation and Bax-mediated apoptosis via the mitochondria. Cisplatin 30-39 BCL2 associated X, apoptosis regulator Homo sapiens 204-207 21052098-4 2011 We demonstrated that Ad-ING4 plus CDDP induced synergistic growth inhibition, enhanced apoptosis, and had an additive effect on upregulation of Fas, Bax, Bak, cleaved Bid, cleaved caspase-8, caspase-9, caspase-3 and cleaved PARP, and on downregulation of Bcl-2 and Bcl-X(L) in SMMC-7721 hepatocarcinoma cells. Cisplatin 34-38 BCL2 associated X, apoptosis regulator Homo sapiens 149-152 22207897-5 2011 Knockdown of miR-203 following cisplatin treatment enhances p53, p21, and Bax protein expression. Cisplatin 31-40 BCL2 associated X, apoptosis regulator Homo sapiens 74-77 21160028-10 2011 These MEFs were more sensitive to cisplatin-induced Bax activation, release of cytochrome c, and apoptosis. Cisplatin 34-43 BCL2 associated X, apoptosis regulator Homo sapiens 52-55 21214929-8 2011 RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2. Cisplatin 58-62 BCL2 associated X, apoptosis regulator Homo sapiens 288-291 21156403-3 2010 We aimed at investigating if the pro-apoptotic members Bad, Bax, Bim and Bid are involved in cisplatin-resistance. Cisplatin 93-102 BCL2 associated X, apoptosis regulator Homo sapiens 60-63 20654585-8 2010 Although, cisplatin-induced apoptosis was associated with the translocation of Bax to mitochondria, release of cytochrome c and caspase-3/7 activation, the levels of relocalized Bax and cytochrome c were significantly greater following GSTP1 knockdown. Cisplatin 10-19 BCL2 associated X, apoptosis regulator Homo sapiens 79-82 20654585-8 2010 Although, cisplatin-induced apoptosis was associated with the translocation of Bax to mitochondria, release of cytochrome c and caspase-3/7 activation, the levels of relocalized Bax and cytochrome c were significantly greater following GSTP1 knockdown. Cisplatin 10-19 BCL2 associated X, apoptosis regulator Homo sapiens 178-181 20372863-7 2010 Cisplatin treatment induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK expression, and suppressed Bcl-2 and Bcl-xl expression, whereas cells transfected with pcDNA3.1-ARL6IP1 showed lower levels of cisplatin-induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK up-regulation and higher levels of cisplatin-suppressed Bcl-2 and Bcl-xl down-regulation. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 48-51 20372863-8 2010 These novel findings collectively suggest that ARL6IP1 may play a key role in cisplatin-induced apoptosis in CaSki cervical cancer cells by regulating the expression of apoptosis-associated proteins such as caspase-3, -9, p53, NF-kappaB, MAPK, Bcl-2, Bcl-xl, and Bax. Cisplatin 78-87 BCL2 associated X, apoptosis regulator Homo sapiens 263-266 20372863-7 2010 Cisplatin treatment induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK expression, and suppressed Bcl-2 and Bcl-xl expression, whereas cells transfected with pcDNA3.1-ARL6IP1 showed lower levels of cisplatin-induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK up-regulation and higher levels of cisplatin-suppressed Bcl-2 and Bcl-xl down-regulation. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 237-240 20100536-8 2010 Moreover, immunoblot analysis indicated that the co-activation of pro-apoptotic factors Bax and p21 were observed in the p73 alpha infected cells after cisplatin treatment. Cisplatin 152-161 BCL2 associated X, apoptosis regulator Homo sapiens 88-91 19821098-6 2009 After cisplatin was added, the expression levels of Bcl-2 mRNA were reduced, and those of Bax, caspase-3, and survivin mRNA were increased in transfection group as compared with those in control group (P<0.05). Cisplatin 6-15 BCL2 associated X, apoptosis regulator Homo sapiens 90-93 20407239-8 2010 Western blot analysis showed that quinacrine plus cisplatin significantly down-regulated cIAP-1 and up-regulated Bax and cleaved caspase-3 expression in Hela and SCC-VII cells compared with single-agent treatment. Cisplatin 50-59 BCL2 associated X, apoptosis regulator Homo sapiens 113-116 19889954-6 2010 During cisplatin treatment, Bax translocated to mitochondria, leading to cytochrome c release. Cisplatin 7-16 BCL2 associated X, apoptosis regulator Homo sapiens 28-31 19910452-10 2010 MDA-7/IL-24 toxicity was enhanced in a weak additive fashion by paclitaxel; paclitaxel enhanced MDA-7/IL-24 + cisplatin lethality in a greater than additive fashion via BAX. Cisplatin 110-119 BCL2 associated X, apoptosis regulator Homo sapiens 169-172 19821098-7 2009 It was concluded that shRNA expression vector targeting Livin gene could inhibit the expression of Livin gene in HeLa cells and enhance the apoptosis induced by cisplatin, which was related to the decreased expression of Bcl-2 and activation of Bax and caspase-3. Cisplatin 161-170 BCL2 associated X, apoptosis regulator Homo sapiens 245-248 20196784-5 2009 The mechanisms underlying the protective effect of autophagy apparently involved the interference with cisplatin-induced modulation of Bcl-2 family proteins, as inhibition of autophagy potentiated cisplatin-mediated up-regulation of proapoptotic Bax and down-regulation of anti-apoptotic Bcl-2. Cisplatin 197-206 BCL2 associated X, apoptosis regulator Homo sapiens 246-249 19724896-9 2009 Our results indicate that SNPs in DNA repair genes (XRCC3241 and XPD751) influence the ICS and together with the expression of EGFR, Hsp70, Bax, and Bcl-2, they could predict the cisplatin sensitivity of head and neck cancer cell lines (r=0.614, p<or=0.001). Cisplatin 179-188 BCL2 associated X, apoptosis regulator Homo sapiens 140-143 19276256-10 2009 Furthermore, the combination of lexatumumab and cisplatin significantly enhanced caspase-8 activity, Bid cleavage, up-regulation of Bax, cytochrome c release, and caspase-9, caspase-6, and caspase-3 activities. Cisplatin 48-57 BCL2 associated X, apoptosis regulator Homo sapiens 132-135 19513519-5 2009 Consistent with these results, the protein levels of Bax and phospho-Bcl-2 increased and those of Bcl-2 and XIAP decreased in cells treated with beta-elemene in combination with cisplatin, compared with the levels in cells treated with either agent alone. Cisplatin 178-187 BCL2 associated X, apoptosis regulator Homo sapiens 53-56 17619073-7 2007 Similar to function way of SM, cDDP causes cancer cell apoptosis though caspase-8/caspase-3 and Bax/cytochrome c pathways, but the resistance to cDDP is correlated with Bcl-2 and Bcl-xL overexpression. Cisplatin 31-35 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 19177004-9 2009 Importantly, HeLa cells with reduced level of Plk1, which induces an increase of p21, p73 and Bax, are more sensitive to some chemotherapeutic agents, such as cisplatin. Cisplatin 159-168 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 18480997-9 2008 Western blotting showed that cisplatin decreased protein expression of E6 and increased protein expression of p53, p21 and Bax. Cisplatin 29-38 BCL2 associated X, apoptosis regulator Homo sapiens 123-126 18992762-7 2009 DMTU also inhibited the CDDP-induced increment of Bax, a pro-apoptotic protein, in the fraction of organelles/membranes at day 3. Cisplatin 24-28 BCL2 associated X, apoptosis regulator Homo sapiens 50-53 18391982-4 2008 As the mechanism, triptolide suppressed CDDP-induced p53 transcriptional activity, leading to p21 attenuation, which promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and Bax. Cisplatin 40-44 BCL2 associated X, apoptosis regulator Homo sapiens 192-195 18566213-0 2008 Trichostatin A up-regulates p73 and induces Bax-dependent apoptosis in cisplatin-resistant ovarian cancer cells. Cisplatin 71-80 BCL2 associated X, apoptosis regulator Homo sapiens 44-47 18191995-6 2008 Real-time PCR was used for gene expression analysis of the TRAIL receptor dr5 and the pro-apoptotic bax following treatment with cisplatin. Cisplatin 129-138 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 17619073-9 2007 The combined treatment of SM and cDDP significantly reduced Bcl-2 and Bcl-xL expressions, and enhanced Bax, cytochrome c, caspase-9 and -3 expressions in breast cancer cells. Cisplatin 33-37 BCL2 associated X, apoptosis regulator Homo sapiens 103-106 17611411-4 2007 This sensitization of cisplatin-induced apoptosis was associated with upregulation of p53, Bax and p21 in U2OS cells. Cisplatin 22-31 BCL2 associated X, apoptosis regulator Homo sapiens 91-94 17582213-8 2007 RESULTS: The expression of CDKN1A, BAX, TNFSF8, and RRM2B was consistently upregulated by CRT (9 Gy with a single administration of cisplatin). Cisplatin 132-141 BCL2 associated X, apoptosis regulator Homo sapiens 35-38 17634542-10 2007 CONCLUSIONS: Low expression of Bax was significantly associated with the poor survival of patients with locally advanced esophageal cancer treated with chemoradiotherapy using 5-fluorouracil and cisplatin. Cisplatin 195-204 BCL2 associated X, apoptosis regulator Homo sapiens 31-34 17130128-9 2007 Nutlin-3 attenuated cisplatin-induced oligomerization of Bax and Bak but not their interactions with Bcl-XL. Cisplatin 20-29 BCL2 associated X, apoptosis regulator Homo sapiens 57-60 16009487-0 2006 Upregulation of Bcl-2 is associated with cisplatin-resistance via inhibition of Bax translocation in human bladder cancer cells. Cisplatin 41-50 BCL2 associated X, apoptosis regulator Homo sapiens 80-83 16894566-6 2006 Aurora-A inhibits cytochrome C release and Bax conformational change induced by CDDP. Cisplatin 80-84 BCL2 associated X, apoptosis regulator Homo sapiens 43-46 16009487-6 2006 Western blot analysis of subcellular fractions showed that cisplatin induced redistribution of Bax and cytochrome c. Cisplatin 59-68 BCL2 associated X, apoptosis regulator Homo sapiens 95-98 16009487-8 2006 In contrast, overexpressed Bcl-2 protein inhibited cisplatin-induced Bax translocation and its downstream events in T24R2. Cisplatin 51-60 BCL2 associated X, apoptosis regulator Homo sapiens 69-72 16012788-0 2005 Enhanced P53 and BAX gene expression and apoptosis in A549 cells by cis-Pt(II) complex of 3-aminoflavone in comparison with cis-DDP. Cisplatin 68-78 BCL2 associated X, apoptosis regulator Homo sapiens 17-20 16082193-11 2005 Cisplatin also acts by increasing pro-apoptotic Bax concentration in the cells thereby leading to caspase-9 activation via the mitochondrial pathway. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 48-51 15790433-12 2005 These alterations conferred cisplatin resistance to cisplatin through the activation of PI3K/Akt and the inhibition of Bax translocation. Cisplatin 28-37 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 16054560-7 2005 In 5 microM cisplatin, expression of HeLa Xrel3 enhanced apoptosis by significantly increasing the expression of the apoptotic proteins Bax and MDM-2 (P<0.05). Cisplatin 12-21 BCL2 associated X, apoptosis regulator Homo sapiens 136-139 15920103-8 2005 Transcriptional activation of p21(WAF1/CIP1) and Bax by p53 on exposure to cisplatin was completely blocked by introducing the p53 decoy oligonucleotide. Cisplatin 75-84 BCL2 associated X, apoptosis regulator Homo sapiens 49-52 15790433-12 2005 These alterations conferred cisplatin resistance to cisplatin through the activation of PI3K/Akt and the inhibition of Bax translocation. Cisplatin 52-61 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 15642728-9 2005 Because knockdown of Bax expression by gene silencing results in prolonged cell survival following treatment with cisplatin in the absence or presence of nicotine, Bax may be an essential component in the nicotine survival signaling pathway. Cisplatin 114-123 BCL2 associated X, apoptosis regulator Homo sapiens 21-24 15642728-9 2005 Because knockdown of Bax expression by gene silencing results in prolonged cell survival following treatment with cisplatin in the absence or presence of nicotine, Bax may be an essential component in the nicotine survival signaling pathway. Cisplatin 114-123 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 15735033-5 2005 The increased cisplatin sensitivity in MAD2 transfectants was associated with mitotic arrest and activation of apoptosis pathway evidenced by the increased mitotic index and apoptosis rate as well as decreased Bcl-2 and Bax ratio and expression of cleaved poly(ADP-ribose) polymerase and caspase 3. Cisplatin 14-23 BCL2 associated X, apoptosis regulator Homo sapiens 220-223 15386344-4 2004 Further, upon cDDP treatment, the levels of Fas, Bax and Bid remained unchanged, whereas Bcl-2 and p-Bad were reduced at late times (120 hr) after treatment. Cisplatin 14-18 BCL2 associated X, apoptosis regulator Homo sapiens 49-52 15604295-7 2004 CDDP treatment induced the activation and redistribution of cytosolic Bax and the release of cytochrome c from injured mitochondria. Cisplatin 0-4 BCL2 associated X, apoptosis regulator Homo sapiens 70-73 15496615-4 2005 Cisplatin cytotoxicity was associated with nuclear translocation of apoptosis induction factor, expression of the pro-apoptotic Bax protein, cleavage of caspases 3 and 9, and cleavage of PARP. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 128-131 14534679-9 2003 A number of experimental strategies to overcome cisplatin resistance are at the preclinical or clinical level such as introduction of the bax gene, inhibition of the JNK pathway, introduction of a functional p53 gene, treatment of tumors with aldose reductase inhibitors and others. Cisplatin 48-57 BCL2 associated X, apoptosis regulator Homo sapiens 138-141 15153331-8 2004 Indeed, GSH ethyl ester-mediated increase of GSH abrogated apoptosis induced by cisplatin and melphalan by inhibition of Bax/cytochrome c redistribution. Cisplatin 80-89 BCL2 associated X, apoptosis regulator Homo sapiens 121-124 14662026-9 2003 The expression of p53 and Bax protein increased with exposure to CDDP and was enhanced by LMB in HeLa and SiHa cells. Cisplatin 65-69 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 15265716-11 2004 The combination of cisplatin/freezing resulted in a 4-fold increase in the ratio of Bax to Bcl-2 when compared to controls, which represented a 2-fold increase over the 5-FU/freezing-combination model. Cisplatin 19-28 BCL2 associated X, apoptosis regulator Homo sapiens 84-87 14719078-0 2004 Protein levels of p21, p27, cyclin E and Bax predict sensitivity to cisplatin and paclitaxel in head and neck squamous cell carcinomas. Cisplatin 68-77 BCL2 associated X, apoptosis regulator Homo sapiens 41-44 14719078-7 2004 Cells with strong expression of p21, p27, or Bax showed significantly higher sensitivity to cisplatin, and cells with strong expression of Bax or weak expression of cyclin E showed significantly higher sensitivity to paclitaxel. Cisplatin 92-101 BCL2 associated X, apoptosis regulator Homo sapiens 45-48 14512787-7 2003 CDDP-induced apoptosis and secondary necrosis were accompanied by activation of caspase-3 and modulation of Bcl-2 family members Bcl-2 and Bax. Cisplatin 0-4 BCL2 associated X, apoptosis regulator Homo sapiens 139-142 14499626-4 2003 However, in the same cells, cisplatin, a DNA-damaging drug, induced Bak and Bax modulation, mitochondrial depolarization, and nuclear fragmentation. Cisplatin 28-37 BCL2 associated X, apoptosis regulator Homo sapiens 76-79 14512787-9 2003 Flow cytometry, which enables measurement of protein at the single-cell level, revealed that Bcl-2+/Bax- cells were decreased, with a slight concomitant rise in Bcl-2-/Bax+ cells on stimulation with CDDP. Cisplatin 199-203 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 14512787-9 2003 Flow cytometry, which enables measurement of protein at the single-cell level, revealed that Bcl-2+/Bax- cells were decreased, with a slight concomitant rise in Bcl-2-/Bax+ cells on stimulation with CDDP. Cisplatin 199-203 BCL2 associated X, apoptosis regulator Homo sapiens 168-171 12697749-8 2003 Cisplatin-induced Bax conformation change was inhibited by inhibitors or dominant negative forms of JNK and p38. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 18-21 12697749-0 2003 AKT2 inhibition of cisplatin-induced JNK/p38 and Bax activation by phosphorylation of ASK1: implication of AKT2 in chemoresistance. Cisplatin 19-28 BCL2 associated X, apoptosis regulator Homo sapiens 49-52 12749865-2 2003 Here, we studied cisplatin hypersensitivity in FA in relation to the mechanism of PCD in lymphoblastoid cells representing FA groups A and C. In FA cells, a low concentration of cisplatin caused chromatin condensation, phosphatidylserine (PS) externalization, and the expression of an 18-kDa variant of Bax, all indicators of apoptotic cell death, and the latter suggesting the involvement of a mitochondrial route. Cisplatin 178-187 BCL2 associated X, apoptosis regulator Homo sapiens 303-306 12697749-9 2003 In conclusion, our data indicate that AKT2 inhibits cisplatin-induced JNK/p38 and Bax activation through phosphorylation of ASK1 and thus, plays an important role in chemoresistance. Cisplatin 52-61 BCL2 associated X, apoptosis regulator Homo sapiens 82-85 12390742-5 2002 CONCLUSION: Mifepristone may act to enhance the sensitivity of COC1/DDP cells to cisplatin, possibly through regulating Bcl-2 and Bax protein expressions. Cisplatin 81-90 BCL2 associated X, apoptosis regulator Homo sapiens 130-133 12478472-4 2002 The cisplatin-induced protein phosphorylation, not detectable in cells treated with BBR 3464, was associated with RPA phosphorylation, a specific up-regulation of Bax and down-regulation of p21(WAF1). Cisplatin 4-13 BCL2 associated X, apoptosis regulator Homo sapiens 163-166 12644821-1 2003 In cell line studies, BCL-2, BAX, as well as novel MEK1 protein levels have strong influence on ovarian cancer response to cisplatin-based chemotherapy. Cisplatin 123-132 BCL2 associated X, apoptosis regulator Homo sapiens 29-32 12520732-8 2002 CONCLUSIONS: Cisplatin-resistance in human ovarian cancer cell lines may associated with the overexpression of anti-apoptotic protein bcl-2 and downregulation of caspase-3 activity, but not associated with the expression of bax and bcl-xs. Cisplatin 13-22 BCL2 associated X, apoptosis regulator Homo sapiens 224-227 12168083-0 2002 Quantitative analysis of expression levels of bax, bcl-2, and survivin in cancer cells during cisplatin treatment. Cisplatin 94-103 BCL2 associated X, apoptosis regulator Homo sapiens 46-49 12168083-7 2002 The changes in expression levels of three genes (bax, bcl-2, and survivin) during CDDP treatment were evaluated by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Cisplatin 82-86 BCL2 associated X, apoptosis regulator Homo sapiens 49-52 12168083-10 2002 The expression level of bax mRNA significantly increased after 24 h treatment with CDDP in MKN-45 cells and it significantly increased after 12 h treatment with CDDP in LoVo cells. Cisplatin 83-87 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 12168083-10 2002 The expression level of bax mRNA significantly increased after 24 h treatment with CDDP in MKN-45 cells and it significantly increased after 12 h treatment with CDDP in LoVo cells. Cisplatin 161-165 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 12403069-6 2002 The increase in Bax mRNA to Bcl-2 mRNA ratio after treatment with CDDP was suppressed in MDR1-overexpressing cells. Cisplatin 66-70 BCL2 associated X, apoptosis regulator Homo sapiens 16-19 12599692-3 2002 RESULTS: Compared with the blank group, the expression of c-myc and bcl-2 genes was low, while that of the p53, bax genes was high(P < 0.01), and the ratio of bax/bcl-2 significantly increased in both the Aining group and the cisplatin(DDP) group. Cisplatin 229-238 BCL2 associated X, apoptosis regulator Homo sapiens 162-165 11748660-6 2002 The effect of LMP1 on the balance of Bcl-2 and Bax ratio may play a role in inducing susceptibility to cisplatin-induced cell death. Cisplatin 103-112 BCL2 associated X, apoptosis regulator Homo sapiens 47-50 11895373-0 2002 Cisplatin-induced apoptosis of DRG neurons involves bax redistribution and cytochrome c release but not fas receptor signaling. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 52-55 11895373-5 2002 However, cisplatin treatment of DRG caused redistribution of cytosolic bax and mitochondrial release of cytochrome c. Cisplatin 9-18 BCL2 associated X, apoptosis regulator Homo sapiens 71-74 11840333-7 2002 Further, the DNA cross-linking drugs BCNU and cisplatin, but not the microtubule poison vincristine, induced significant cell death in U87MG/hDkk cells, and this was accompanied by altered Bcl-2/Bax expression and a reduction in the amount of telomere DNA as visualized by fluorescence in situ hybridization. Cisplatin 46-55 BCL2 associated X, apoptosis regulator Homo sapiens 195-198 11172605-8 2001 The antitumor effect of 5-FU and CDDP was significantly enhanced in the combination with intra-tumoral administration of bax gene as compared to that of CDDP and 5-FU alone (p<0.05, Student"s t-test). Cisplatin 33-37 BCL2 associated X, apoptosis regulator Homo sapiens 121-124 11761456-4 2001 In the present study, we expanded our investigations to examine the effect of cisplatin-induced ERK activation on the expression of p53-targeted genes that have been shown to be important in the cellular response to DNA damage including Bax, Bcl-2, Bcl-x1, Cyclin G, Gadd45, p21WAF1, and Mdm2. Cisplatin 78-87 BCL2 associated X, apoptosis regulator Homo sapiens 237-240 11340162-2 2001 Because cisplatin-induced modulation of the related Bax protein was seen in only one cell line, a degree of specificity in the signal to Bak is indicated. Cisplatin 8-17 BCL2 associated X, apoptosis regulator Homo sapiens 52-55 11497278-7 2001 Increased expression of bax and reduced expression of bcl-2 are involved in the growth-inhibitory effect of CDDP on pancreatic cancer cells with wild-type p53 gene. Cisplatin 108-112 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 11313183-7 2001 In astrocytoma cells, cisplatin treatment resulted in the upregulation of p53, p21 and bax, while only p21 induction was observed after BBR3464 treatment. Cisplatin 22-31 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 11848465-6 2001 HA-bax clones were significantly more sensitive to cell death induction by cis-diamminedichloroplatinum, etoposide, doxorubicin and gamma-radiation than vector control cells. Cisplatin 75-103 BCL2 associated X, apoptosis regulator Homo sapiens 3-6 11384107-8 2001 In SK-OV-3 cells with transduction of the p53 gene, the expression of p53 and Bax proteins increased after exposure to CDDP. Cisplatin 119-123 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 11401473-6 2001 Accumulation of P53 and its target gene bax then sensitized HeLa cells to cell-cycle arrest, cell death/apoptosis induced by cisplatin, and etoposide. Cisplatin 125-134 BCL2 associated X, apoptosis regulator Homo sapiens 40-43 11267864-3 2001 The cytotoxic effect of Bax was observed in three ovarian cancer cell lines: the per cent reduction in the number of cells was 40.0% for cisplatin-sensitive A2780, 50.0% for cisplatin-resistant A2780/cDDP, and 64.8% for marginally cisplatin-resistant OVCAR-3. Cisplatin 137-146 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 11267864-3 2001 The cytotoxic effect of Bax was observed in three ovarian cancer cell lines: the per cent reduction in the number of cells was 40.0% for cisplatin-sensitive A2780, 50.0% for cisplatin-resistant A2780/cDDP, and 64.8% for marginally cisplatin-resistant OVCAR-3. Cisplatin 174-183 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 11267864-3 2001 The cytotoxic effect of Bax was observed in three ovarian cancer cell lines: the per cent reduction in the number of cells was 40.0% for cisplatin-sensitive A2780, 50.0% for cisplatin-resistant A2780/cDDP, and 64.8% for marginally cisplatin-resistant OVCAR-3. Cisplatin 200-204 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 11267864-3 2001 The cytotoxic effect of Bax was observed in three ovarian cancer cell lines: the per cent reduction in the number of cells was 40.0% for cisplatin-sensitive A2780, 50.0% for cisplatin-resistant A2780/cDDP, and 64.8% for marginally cisplatin-resistant OVCAR-3. Cisplatin 174-183 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 11267864-5 2001 Cisplatin-resistant A2780/cDDP had a p53 mutation and exhibited attenuated Bax induction after cisplatin treatment, which may explain why supplementation of Bax was effective in this chemoresistant ovarian cancer. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 75-78 11267864-5 2001 Cisplatin-resistant A2780/cDDP had a p53 mutation and exhibited attenuated Bax induction after cisplatin treatment, which may explain why supplementation of Bax was effective in this chemoresistant ovarian cancer. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 157-160 11267864-5 2001 Cisplatin-resistant A2780/cDDP had a p53 mutation and exhibited attenuated Bax induction after cisplatin treatment, which may explain why supplementation of Bax was effective in this chemoresistant ovarian cancer. Cisplatin 95-104 BCL2 associated X, apoptosis regulator Homo sapiens 75-78 11267864-5 2001 Cisplatin-resistant A2780/cDDP had a p53 mutation and exhibited attenuated Bax induction after cisplatin treatment, which may explain why supplementation of Bax was effective in this chemoresistant ovarian cancer. Cisplatin 95-104 BCL2 associated X, apoptosis regulator Homo sapiens 157-160 11267864-6 2001 Combination with cisplatin or paclitaxel enhanced the cytotoxic effect of Bax induction in all but one cell line including cisplatin-resistant A2780/cDDP. Cisplatin 17-26 BCL2 associated X, apoptosis regulator Homo sapiens 74-77 11267864-6 2001 Combination with cisplatin or paclitaxel enhanced the cytotoxic effect of Bax induction in all but one cell line including cisplatin-resistant A2780/cDDP. Cisplatin 123-132 BCL2 associated X, apoptosis regulator Homo sapiens 74-77 11123425-5 2000 Apoptosis induced by a chemotherapeutic agent, 5-fluorouracil, mitomycin C, paclitaxel, doxorubicin, or cisplatin, was enhanced by Bax overexpression. Cisplatin 104-113 BCL2 associated X, apoptosis regulator Homo sapiens 131-134 11299769-6 2001 Our results suggest that upregulation of Bax is associated with the sensitivity of these NPC cells to cisplatin. Cisplatin 102-111 BCL2 associated X, apoptosis regulator Homo sapiens 41-44 11125422-16 2001 Treating T24 cells with cisplatin enhanced the expression of bax but not bcl-2. Cisplatin 24-33 BCL2 associated X, apoptosis regulator Homo sapiens 61-64 11175336-4 2000 We found the formation of previously unreported nuclear complexes between the tumor suppressor protein p53 and the pro-apoptotic protein Bax, in human melanoma cell lines induced into apoptosis following cisplatin exposure. Cisplatin 204-213 BCL2 associated X, apoptosis regulator Homo sapiens 137-140 11175336-6 2000 Three channel fluorescence laser scanning confocal image microscopy revealed that the nuclear Bax/p53 complexes remained in the nucleus and localized proximal to DNA fragmentation sites as assayed by TUNEL after cisplatin exposure. Cisplatin 212-221 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 11175336-9 2000 The degree of apoptosis induced by different concentrations of cisplatin correlated with the amount of nuclear Bax/p53 complexes. Cisplatin 63-72 BCL2 associated X, apoptosis regulator Homo sapiens 111-114 10974635-5 2000 After exposure to CDDP, p53 and Bax protein expression increased and Bcl-xL expression decreased in the KF cells and TP53 gene-transducted SK-OV-3 cells. Cisplatin 18-22 BCL2 associated X, apoptosis regulator Homo sapiens 32-35 10024685-5 1999 Bax expression was reduced in spheroids following cisplatin or Taxol treatment, while p53 levels remained unchanged. Cisplatin 50-59 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 10891529-2 2000 We have examined the effect of cisplatin alone and in combination with theophylline, a phoshodiesterase inhibitor, on modulation of Bcl-2/Bax expression and induction of apoptosis in human granulosa cells transformed by stable transfection with mutant p53 plus Ha-ras. Cisplatin 31-40 BCL2 associated X, apoptosis regulator Homo sapiens 138-141 10769693-3 2000 Apoptosis in the bax-transfected gastric cancer cells was enhanced following the treatment of various chemotherapeutic agents including adriamycin (ADM), cisplatin (CDDP), etoposide (VP-16) and taxotere (TXT) as compared to those of neo gene-transfected cells. Cisplatin 154-163 BCL2 associated X, apoptosis regulator Homo sapiens 17-20 10769693-3 2000 Apoptosis in the bax-transfected gastric cancer cells was enhanced following the treatment of various chemotherapeutic agents including adriamycin (ADM), cisplatin (CDDP), etoposide (VP-16) and taxotere (TXT) as compared to those of neo gene-transfected cells. Cisplatin 165-169 BCL2 associated X, apoptosis regulator Homo sapiens 17-20 10769693-7 2000 The tumor growth in the bax-transfected cells was significantly suppressed following the treatment of CDDP or VP-16 compared to that of neo-transfected cells (p < 0.05). Cisplatin 102-106 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 10446454-0 1999 Apoptosis-promoting gene (bax) transfer potentiates sensitivity of squamous cell carcinoma to cisplatin in vitro and in vivo. Cisplatin 94-103 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 10446454-3 1999 To investigate the role of bax gene expression in modulating cisplatin (CDDP)-induced apoptosis in vitro, an established CDDP-resistant human head and neck SCC (IMC-3 cell line) was transfected with bax gene-bearing mammalian expression vector. Cisplatin 72-76 BCL2 associated X, apoptosis regulator Homo sapiens 27-30 10446454-4 1999 Overexpression of the bax gene in CDDP-resistant IMC-3 cells elevated the CDDP susceptibility of tumor cells to a level similar to that of the parental IMC-3 cells. Cisplatin 34-38 BCL2 associated X, apoptosis regulator Homo sapiens 22-25 10446454-4 1999 Overexpression of the bax gene in CDDP-resistant IMC-3 cells elevated the CDDP susceptibility of tumor cells to a level similar to that of the parental IMC-3 cells. Cisplatin 74-78 BCL2 associated X, apoptosis regulator Homo sapiens 22-25 10397248-11 1999 A change in the expression of Mr 24,000 Bax to a Mr 21,000 isoform was evidenced in the A2780 cells within 48 h of cisplatin treatment and, to a greater extent, in the CP70 and C30 cells, which also expressed a Mr 16,000 Bax variant. Cisplatin 115-124 BCL2 associated X, apoptosis regulator Homo sapiens 40-43 10880019-5 2000 Furthermore, Bax-expressing MKN-28 cells were more sensitive to cisplatin. Cisplatin 64-73 BCL2 associated X, apoptosis regulator Homo sapiens 13-16 10762058-0 2000 Enhanced induction of Bax gene expression in H460 and H1299 cells with the combined treatment of cisplatin and adenovirus mediated wt-p53 gene transfer. Cisplatin 97-106 BCL2 associated X, apoptosis regulator Homo sapiens 22-25 10762058-7 2000 These results suggest that cisplatin induced p53 protein phosphorylation and may activate the downstream of p53 gene expression such as p21 and Bax. Cisplatin 27-36 BCL2 associated X, apoptosis regulator Homo sapiens 144-147 10080945-2 1999 The present study demonstrates that the cytotoxic drugs cisplatin, doxorubicin and mitomycin C induce the accumulation of the Fas receptor, the FADD adaptor molecule, the procaspases-8, -3 and -2L and the proapoptotic molecule Bax in several human colon cancer cells. Cisplatin 56-65 BCL2 associated X, apoptosis regulator Homo sapiens 227-230 10063313-0 1999 The relationship between cisplatin-induced apoptosis and p53, bcl-2 and bax expression in human lung cancer cells. Cisplatin 25-34 BCL2 associated X, apoptosis regulator Homo sapiens 72-75 9393748-2 1997 Here, we demonstrate that expression of galectin-3 in human breast carcinoma BT549 cells inhibits cis-diamminedichloroplatinum (cisplatin)-induced poly(ADP-ribose) polymerase degradation and apoptosis, without altering Bcl-2, Bcl-X(L), or Bax expressions. Cisplatin 128-137 BCL2 associated X, apoptosis regulator Homo sapiens 239-242 9635829-0 1998 Expression of p53, Bcl-2 and Bax in cisplatin-induced apoptosis in testicular germ cell tumour cell lines. Cisplatin 36-45 BCL2 associated X, apoptosis regulator Homo sapiens 29-32 9635829-1 1998 We examined the sensitivity for cisplatin-induced apoptosis in a panel of four testicular germ cell tumour (TGCT) cell lines and monitored the cellular expression of the apoptosis-related proteins p53, Bcl-2 and Bax. Cisplatin 32-41 BCL2 associated X, apoptosis regulator Homo sapiens 212-215 9635829-11 1998 The present study suggests that, at least in our panel of TGCT cell lines, hypersensitivity for cisplatin-induced apoptosis might not be necessarily correlated with the presence of wild-type p53 and is probably not associated with Bcl-2 and Bax expression. Cisplatin 96-105 BCL2 associated X, apoptosis regulator Homo sapiens 241-244 9584207-0 1998 Cisplatin- and paclitaxel-induced apoptosis of ovarian carcinoma cells and the relationship between bax and bak up-regulation and the functional status of p53. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 9494534-9 1997 Expression of bcl-2 family members (bax, bcl-x) was modulated by fotemustine, etoposide and cisplatin. Cisplatin 92-101 BCL2 associated X, apoptosis regulator Homo sapiens 36-39 9413185-6 1997 The results suggested that in Panc-1 cells cisplatin and VP-16 induced apoptotic cell death which was mediated through the interaction of Bax expression in the presence of mutated p53. Cisplatin 43-52 BCL2 associated X, apoptosis regulator Homo sapiens 138-141 9815594-7 1997 The expression of Bcl-2 relative to Bax decreased more after combined treatment with cisplatin and ATRA than after either drug alone. Cisplatin 85-94 BCL2 associated X, apoptosis regulator Homo sapiens 36-39 9212237-7 1997 At the same time, we found strong induction of p53, waf-1 and bax protein levels after CDDP treatment in the A2780, but not in the A2780-DX3, cell line. Cisplatin 87-91 BCL2 associated X, apoptosis regulator Homo sapiens 62-65 9041117-0 1997 Bax upregulation is an early event in cisplatin-induced apoptosis in human testicular germ-cell tumor cell line NT2, as quantitated by flow cytometry. Cisplatin 38-47 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 8798452-0 1996 Bax can antagonize Bcl-XL during etoposide and cisplatin-induced cell death independently of its heterodimerization with Bcl-XL. Cisplatin 47-56 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 9306577-0 1997 Overexpression of bax sensitizes breast cancer MCF-7 cells to cisplatin and etoposide. Cisplatin 62-71 BCL2 associated X, apoptosis regulator Homo sapiens 18-21 8798452-4 1996 Expression of wild-type Bax countered the repressor activity of Bcl-XL against cell death mediated by VP-16 and cisplatin. Cisplatin 112-121 BCL2 associated X, apoptosis regulator Homo sapiens 24-27 33773191-11 2021 DS-1 treatment in combination with cisplatin could enhance activated p-p53 (Ser15) and p53 downstream signaling (Bax, Bcl-2, and Akt), leading to a higher level of apoptosis. Cisplatin 35-44 BCL2 associated X, apoptosis regulator Homo sapiens 113-116 8798452-11 1996 Therefore, Bax can antagonize Bcl-XL during VP-16 and, in a lesser degree, during cisplatin-induced cell death independent of its heterodimerization with Bcl-XL. Cisplatin 82-91 BCL2 associated X, apoptosis regulator Homo sapiens 11-14 8564971-0 1996 Association between cisplatin resistance and mutation of p53 gene and reduced bax expression in ovarian carcinoma cell systems. Cisplatin 20-29 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 8564971-11 1996 Northern blot analysis demonstrated a marked reduction in bax mRNA levels in IGROV-1/Pt 1 cisplatin-resistant cells. Cisplatin 90-99 BCL2 associated X, apoptosis regulator Homo sapiens 58-61 8564971-13 1996 Taken together, these observations support a role for mutations of the p53 gene in the development of cisplatin resistance in ovarian cancer as a consequence of loss of the ability of p53 to transactivate bax, an apoptosis-inducing gene. Cisplatin 102-111 BCL2 associated X, apoptosis regulator Homo sapiens 205-208 34876239-5 2021 However, the expression levels of other tumor-related factors, including Ki67, p27, p53, Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), caspase-3 (Cas-3), matrix metallopeptidase 2 (MMP2) and vascular endothelial growth factor (VEGF) proteins, were constantly maintained in the tumors of all three substrains after cisplatin treatment. Cisplatin 329-338 BCL2 associated X, apoptosis regulator Homo sapiens 89-115 34974280-10 2022 The evidence indicated that CDDP could significantly increase Bax and Bad expression and activate caspase-3 cascade in OLFM4-depleted GBC cells through ARL6IP1. Cisplatin 28-32 BCL2 associated X, apoptosis regulator Homo sapiens 62-65 34876239-5 2021 However, the expression levels of other tumor-related factors, including Ki67, p27, p53, Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), caspase-3 (Cas-3), matrix metallopeptidase 2 (MMP2) and vascular endothelial growth factor (VEGF) proteins, were constantly maintained in the tumors of all three substrains after cisplatin treatment. Cisplatin 329-338 BCL2 associated X, apoptosis regulator Homo sapiens 117-120 35398618-9 2022 Consistently, Nanog suppression combined with Cisplatin led to upregulation of Caspase-3 apoptotic gene and Bax/Bcl-2 ratio. Cisplatin 46-55 BCL2 associated X, apoptosis regulator Homo sapiens 108-111 34183962-10 2021 Piperine (20 muM) and cisplatin (5 muM) for 24 h induce apoptosis strongly through reduction of Bcl-2 and increase of caspase 3, p53, caspase 9, and Bax. Cisplatin 22-31 BCL2 associated X, apoptosis regulator Homo sapiens 149-152 35500680-9 2022 Low concentrations of 4 mug/ml cisplatin and 2.8 mug/ml sunitinib showed significant Bcl-2 down-regulation and Bax up-regulation. Cisplatin 31-40 BCL2 associated X, apoptosis regulator Homo sapiens 111-114 35525317-0 2022 Cisplatin-induced pyroptosis is mediated via the CAPN1/CAPN2-BAK/BAX-caspase-9-caspase-3-GSDME axis in esophageal cancer. Cisplatin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 65-68 35525317-11 2022 Mechanistically, we uncovered a novel mechanism whereby cisplatin induced pyroptosis via activation of a CAPN1/CAPN2-BAK/BAX-caspase-9-caspase-3-GSDME signaling axis in esophageal cancer cells. Cisplatin 56-65 BCL2 associated X, apoptosis regulator Homo sapiens 121-124 35608496-11 2022 Agmatine did not significantly reduce the cisplatin-induced increase in reactive oxygen species but decreased the expression of BCL2-associated X protein and the activity of caspase-3. Cisplatin 42-51 BCL2 associated X, apoptosis regulator Homo sapiens 128-153 34549307-8 2021 The results revealed that SPHK1 was positively correlated with cisplatin resistance in bladder cancer cells, exhibiting an antiapoptotic effect that was reflected by the downregulation of apoptosis-related proteins (Bax and cleaved caspase-3) and the upregulation of an antiapoptotic protein (Bcl-2) in SPHK1-overexpression cell lines. Cisplatin 63-72 BCL2 associated X, apoptosis regulator Homo sapiens 216-219 34080212-0 2021 Combination of cyanidin-3-O-glucoside and cisplatin induces oxidative stress and apoptosis in HeLa cells by reducing activity of endogenous antioxidants, increasing bax/bcl-2 mRNA expression ratio, and downregulating Nrf2 expression. Cisplatin 42-51 BCL2 associated X, apoptosis regulator Homo sapiens 165-168 34149993-8 2021 The mAb against MOR also enhanced the cisplatin-induced apoptosis of HCC cells by downregulating p-ERK, Bcl-2 and upregulating Bax. Cisplatin 38-47 BCL2 associated X, apoptosis regulator Homo sapiens 127-130 34522245-11 2021 After cisplatin treatment, down-regulation of BANCR could consequently attenuate TU686-DDP-R and TU177-DDP-R cell proliferation, and the expression of MRP1, Bcl-2, and p-PKB was decreased and Bax was increased. Cisplatin 6-15 BCL2 associated X, apoptosis regulator Homo sapiens 192-195 35136652-5 2022 The ieSCI-chip successfully identified a subgroup of apoptosis-negative (Bax-negative) cells, which traditional bulk analysis did not detect, from cisplatin-treated cells. Cisplatin 147-156 BCL2 associated X, apoptosis regulator Homo sapiens 73-76 35433741-11 2022 Meanwhile, the enhanced protein levels of Bax, cleaved caspase-3/caspase-3 ratio, levels of Pp-65/p-65, levels of IL-6, and the production of ROS induced by cisplatin were significantly attenuated by ISL treatment. Cisplatin 157-166 BCL2 associated X, apoptosis regulator Homo sapiens 42-45 33719846-12 2021 Baicalin enhanced the effect of cisplatin on promoting apoptosis, arresting cell on S stage and triggering DNA damage accompanied with the upregulation of Bcl-2-associated X protein (Bax) and downregulation of B-cell lymphoma 2 (Bcl-2) and Cyclin D1 in A549/DPP cells. Cisplatin 32-41 BCL2 associated X, apoptosis regulator Homo sapiens 183-186 34994335-10 2022 These compounds combined with cisplatin caused upregulation in the pro-apoptotic Bax, Bid, caspase-3, caspase-8, caspase-9, Fas, and p53 gene expressions while downregulating anti-apoptotic DFFA, NFkB1, and Bcl2 gene expressions. Cisplatin 30-39 BCL2 associated X, apoptosis regulator Homo sapiens 81-84 33945910-0 2021 Captopril downregulates expression of Bax/cytochrome C/caspase-3 apoptotic pathway, reduces inflammation, and oxidative stress in cisplatin-induced acute hepatic injury. Cisplatin 130-139 BCL2 associated X, apoptosis regulator Homo sapiens 38-41 32757998-9 2021 Simultaneous treatment with the extract and cisplatin increased the latter"s cytotoxicity, apoptotic cell death, and BAX expression in HepG2 cells. Cisplatin 44-53 BCL2 associated X, apoptosis regulator Homo sapiens 117-120 33569751-11 2021 Our results showed that miRNA-143 overexpression could increase cisplatin-induced apoptosis and increase the sensitivity of CaSki cells to low doses of this chemotherapeutic agent via modulating the expression of apoptosis-related genes including Bcl-2, Bax, and caspase-9. Cisplatin 64-73 BCL2 associated X, apoptosis regulator Homo sapiens 254-257 33126443-9 2020 Linalool mitigated cisplatin-induced apoptotic markers such as caspase 3, caspase 9, and Bax expression, and boosted the anti-apoptotic Bcl2 expression. Cisplatin 19-28 BCL2 associated X, apoptosis regulator Homo sapiens 89-92 33390811-0 2021 LncRNA XIST acts as a MicroRNA-520 sponge to regulate the Cisplatin resistance in NSCLC cells by mediating BAX through CeRNA network. Cisplatin 58-67 BCL2 associated X, apoptosis regulator Homo sapiens 107-110 33390811-16 2021 Conclusions: LncRNA XIST competitively bound to miRNA 520 in the regulation of cisplatin resistance by BAX, participating apoptosis in the p53 signaling pathway. Cisplatin 79-88 BCL2 associated X, apoptosis regulator Homo sapiens 103-106 33402832-9 2020 Western blot assay revealed that expression of pro-apoptosis protein Bax and C-Caspase 3 increased, but apoptosis-inhibitory protein Bcl-2 expression decreased with 40 mug/mL cis-platinum, 12.5 mug/mL allicin, 25 mug/mL allicin, and 50 mug/mL allicin, while compared to 40 mug/mL cis-platinum, Bax and C-Caspase 3 expression was increased by 50 mug/mL allicin. Cisplatin 175-187 BCL2 associated X, apoptosis regulator Homo sapiens 294-297 33038371-11 2020 Moreover, higher antitumor activity was observed in the combined group than that in cisplatin alone, which could be reflected by the number of apoptotic cells in tumor tissues and over expression of bax in the combined group. Cisplatin 84-93 BCL2 associated X, apoptosis regulator Homo sapiens 199-202 32947166-8 2020 Moreover, the acetazolamide/cisplatin combination could decrease the level of PCNA but increase the level of p53; decrease the ratio of Bcl-2/Bax and increase the expression of caspase-3 compared with the single drug treated group. Cisplatin 28-37 BCL2 associated X, apoptosis regulator Homo sapiens 142-145 32044796-8 2020 C61-LNP, as well as C61-LNP + CDDP treatments, caused pro-apoptotic proteomic changes including an increase in cleaved fragments of caspases-3 and -9 consistent with caspase activation as well as an improvement in the anti-apoptotic Bcl2 and Bax levels. Cisplatin 30-34 BCL2 associated X, apoptosis regulator Homo sapiens 242-245 32374939-7 2020 More importantly, the cisplatin-induced elevated protein levels of Bax, cleaved caspase-3, cleaved caspase-9, and decreased protein level of Bcl-2 were reversed after treatment with Rk1. Cisplatin 22-31 BCL2 associated X, apoptosis regulator Homo sapiens 67-70 32878788-8 2020 Butyl-Pt, pentyl-Pt and cisplatin arrested the cell cycle in the S-phase and induced apoptotic cell death via regulation of expression of B-cell lymphoma 2 (BCL2) and BCL2-associated X (BAX) proteins. Cisplatin 24-33 BCL2 associated X, apoptosis regulator Homo sapiens 167-184 32878788-8 2020 Butyl-Pt, pentyl-Pt and cisplatin arrested the cell cycle in the S-phase and induced apoptotic cell death via regulation of expression of B-cell lymphoma 2 (BCL2) and BCL2-associated X (BAX) proteins. Cisplatin 24-33 BCL2 associated X, apoptosis regulator Homo sapiens 186-189 32973533-11 2020 DDP and hesperetin also induced significant increases in apoptosis inducing factor (AIF), BCL2 associated X, apoptosis regulator (BAX), cleaved caspase-9, and cleaved caspase-3, and decreased B-cell lymphoma 2 (BCL2), caspase-9, and caspase-3 levels. Cisplatin 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 90-128 32973533-11 2020 DDP and hesperetin also induced significant increases in apoptosis inducing factor (AIF), BCL2 associated X, apoptosis regulator (BAX), cleaved caspase-9, and cleaved caspase-3, and decreased B-cell lymphoma 2 (BCL2), caspase-9, and caspase-3 levels. Cisplatin 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 130-133 32124583-11 2020 Our data revealed that silencing of CCAT1 promoted cisplatin-induced apoptosis via modulating the expression of pro- or anti-apoptotic proteins Bax, Bcl-2 and survivin. Cisplatin 51-60 BCL2 associated X, apoptosis regulator Homo sapiens 144-147 32653124-7 2020 Furthermore, the mRNA expression of Caspase 3 was down-regulated significantly and the ratio of Bcl-2/Bax was up-regulated significantly in EVs + CDDP group. Cisplatin 146-150 BCL2 associated X, apoptosis regulator Homo sapiens 102-105