PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28797284-9 2017 Western blot results demonstrated that gambogic acid sensitized gemcitabine-induced apoptosis by enhancing the expression of cleaved caspase-3, cleaved caspase-9, cleaved-PARP, and Bax, and reducing the expression of Bcl-2. gemcitabine 64-75 BCL2 associated X, apoptosis regulator Homo sapiens 181-184 28055291-7 2017 Western blot analysis also demonstrated a significantly reduced level of cyclin D1, Bcl-2, and an obviously increase level of Bax and full-length caspase-3 in A549, NCI-H460 and NCI-H520 cells treated with metuzumab/gemcitabine combination in comparison with single agent treated cells. gemcitabine 216-227 BCL2 associated X, apoptosis regulator Homo sapiens 126-129 27459907-3 2016 Such pretreatment led to significant induction of pro-apoptosis proteins, including caspase-3, cleaved-PARP and Bax (P<0.05), after lower doses of gemcitabine compared to monotherapy. gemcitabine 150-161 BCL2 associated X, apoptosis regulator Homo sapiens 112-115 25833690-3 2015 Herein, we sought to investigate the impact of gemcitabine on the expression levels of the BCL2 family members BCL2, BAX, and BCL2L12 and the apoptosis-related microRNAs miR-182, miR-96, miR-145, and miR-16 in the human bladder and kidney cancer cell lines T24 and Caki-1, respectively. gemcitabine 47-58 BCL2 associated X, apoptosis regulator Homo sapiens 117-120 25344906-7 2015 Thymoquinone pretreatment and gemcitabine also induced down-regulation of anti-apoptotic Bcl-2, Bcl-xL, XIAP and up-regulation and activation of pro-apoptotic molecules including Caspase-3, Caspase-9, Bax and increased release of cytochrome c. gemcitabine 30-41 BCL2 associated X, apoptosis regulator Homo sapiens 201-204 25880226-0 2015 pERK1/2 silencing sensitizes pancreatic cancer BXPC-3 cell to gemcitabine-induced apoptosis via regulating Bax and Bcl-2 expression. gemcitabine 62-73 BCL2 associated X, apoptosis regulator Homo sapiens 107-110 25880226-3 2015 It has also shown that Bcl-2 confers resistance and Bax sensitizes to gemcitabine-induced apoptosis in pancreatic cancer cells. gemcitabine 70-81 BCL2 associated X, apoptosis regulator Homo sapiens 52-55 25880226-5 2015 We therefore tested the hypothesis that pancreatic cancer cells are resistant to gemcitabine and this resistance is due to activation of ERK1/2 and subsequent upregulation of Bcl-2 and downregulation of Bax. gemcitabine 81-92 BCL2 associated X, apoptosis regulator Homo sapiens 203-206 25880226-13 2015 Combined treatment with PD98059 and Bax siRNA transfection could decrease gemcitabine-induced ERK1/2 and Bax activation, which subsequently resulted in decreased apoptosis. gemcitabine 74-85 BCL2 associated X, apoptosis regulator Homo sapiens 36-39 25880226-13 2015 Combined treatment with PD98059 and Bax siRNA transfection could decrease gemcitabine-induced ERK1/2 and Bax activation, which subsequently resulted in decreased apoptosis. gemcitabine 74-85 BCL2 associated X, apoptosis regulator Homo sapiens 105-108 25880226-14 2015 CONCLUSIONS: The upregulation of ERK1/2-dependent Bcl-2 and downregulation of ERK1/2-dependent Bax can protect human pancreatic cancer cells from gemcitabine-induced apoptosis. gemcitabine 146-157 BCL2 associated X, apoptosis regulator Homo sapiens 95-98 25880226-15 2015 Targeting the ERK1/2-Bax/Bcl-2 pathway may in part lead to sensitization of pancreatic cancer to gemcitabine. gemcitabine 97-108 BCL2 associated X, apoptosis regulator Homo sapiens 21-24 25242370-6 2014 Western blot and quantitative polymerase chain reaction analyses demonstrated that the expression levels of the anti-apoptotic gene Bcl-2 and the Bcl-2/Bax ratio in the oridonin and the oridonin plus gemcitabine groups were significantly downregulated as compared with the gemcitabine treatment and control groups. gemcitabine 200-211 BCL2 associated X, apoptosis regulator Homo sapiens 152-155 25242370-8 2014 The results suggested that oridonin improved the anti-tumor effects of gemcitabine through the enhancement of gemcitabine-induced apoptosis.This mechanism may be through the downregulation of Bcl-2 expression and the upregulation of Bax expression, resulting in the reduction of the Bcl-2/Bax ratio. gemcitabine 71-82 BCL2 associated X, apoptosis regulator Homo sapiens 233-236 25242370-8 2014 The results suggested that oridonin improved the anti-tumor effects of gemcitabine through the enhancement of gemcitabine-induced apoptosis.This mechanism may be through the downregulation of Bcl-2 expression and the upregulation of Bax expression, resulting in the reduction of the Bcl-2/Bax ratio. gemcitabine 71-82 BCL2 associated X, apoptosis regulator Homo sapiens 289-292 25242370-8 2014 The results suggested that oridonin improved the anti-tumor effects of gemcitabine through the enhancement of gemcitabine-induced apoptosis.This mechanism may be through the downregulation of Bcl-2 expression and the upregulation of Bax expression, resulting in the reduction of the Bcl-2/Bax ratio. gemcitabine 110-121 BCL2 associated X, apoptosis regulator Homo sapiens 233-236 25242370-8 2014 The results suggested that oridonin improved the anti-tumor effects of gemcitabine through the enhancement of gemcitabine-induced apoptosis.This mechanism may be through the downregulation of Bcl-2 expression and the upregulation of Bax expression, resulting in the reduction of the Bcl-2/Bax ratio. gemcitabine 110-121 BCL2 associated X, apoptosis regulator Homo sapiens 289-292 24804820-8 2014 Furthermore, as shown by our results, the inhibition of gemcitabine-induced autophagy by chloroquine shifts the expression of the p53 protein, Bcl-2 family proteins and the relative Bax/Bcl-xL ratio in favor of promoting apoptosis. gemcitabine 56-67 BCL2 associated X, apoptosis regulator Homo sapiens 182-185 24619961-6 2014 Combined treatment of berbamine and gemcitabine resulted in down-regulation of anti-apoptotic proteins (Bcl-2, Bcl-xL) and up-regulation of pro-apoptotic proteins (Bax, Bid). gemcitabine 36-47 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 24998655-8 2014 The inhibition rates of gemcitabine treated-cells were significantly higher in Notch1 siRNA transfection groups than in corresponding siRNA control groups (AsPC-1: 67.5+-6.7 vs 47.5+-6.8; BxPC-3: 90.5+-4.4 vs 70.2+-4.2; MIAPaCa-2: 80.9+-5.7 vs 58.1+-6.0; Ps<0.05), with the overexpression of protein Bax. gemcitabine 24-35 BCL2 associated X, apoptosis regulator Homo sapiens 303-306 24216611-0 2014 MiR-365 induces gemcitabine resistance in pancreatic cancer cells by targeting the adaptor protein SHC1 and pro-apoptotic regulator BAX. gemcitabine 16-27 BCL2 associated X, apoptosis regulator Homo sapiens 132-135 24216611-8 2014 The siRNA-based knockdown of SHC1 and BAX increased gemcitabine resistance, indicating the miR-365/SHC1/BAX axis influences the survival of pancreatic cancer cells. gemcitabine 52-63 BCL2 associated X, apoptosis regulator Homo sapiens 38-41 24216611-8 2014 The siRNA-based knockdown of SHC1 and BAX increased gemcitabine resistance, indicating the miR-365/SHC1/BAX axis influences the survival of pancreatic cancer cells. gemcitabine 52-63 BCL2 associated X, apoptosis regulator Homo sapiens 104-107 24014050-0 2014 The role of Bax and Bcl-2 in gemcitabine-mediated cytotoxicity in uveal melanoma cells. gemcitabine 29-40 BCL2 associated X, apoptosis regulator Homo sapiens 12-15 22573342-10 2012 RAP80 siRNA combined with gemcitabine significantly increased (P < 0.01) apoptosis of pancreatic cancer cell lines SW1990 and Capan-2, increased expression of Bax mRNA, reduced Bcl-2 mRNA expression (P < 0.01), and slightly increased TRAIL mRNA expression (P < 0.01). gemcitabine 26-37 BCL2 associated X, apoptosis regulator Homo sapiens 162-165 22573342-11 2012 Correspondingly, in the RAP80 siRNA combined with gemcitabine group, both Bax and cleaved caspase-8 protein levels were increased (P < 0.01), whereas Bcl-2 protein decreased significantly (P < 0.01). gemcitabine 50-61 BCL2 associated X, apoptosis regulator Homo sapiens 74-77 22679728-10 2012 The protein expression of Bax was up-regulated and that of Bcl-2 down-regulated in the emodin group and the emodin combined gemcitabine group when compared with the control group (P < 0.05). gemcitabine 124-135 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 22679728-11 2012 Emodin combined with gemcitabine could significantly inhibit the growth of pancreatic xenograft tumors, increase the positive expression of Bax in tumor tissues, obviously decrease the positive expressions of Ki-67 and Bcl-2 (P < 0.05). gemcitabine 21-32 BCL2 associated X, apoptosis regulator Homo sapiens 140-143 22679728-13 2012 CONCLUSION: Emodin could potentiate the inhibition of pancreatic cancer growth induced by gemcitabine both in vitro and in vivo, which might be achieved by up-regulating the expression of Bax and down-regulating the expression of Bcl-2. gemcitabine 90-101 BCL2 associated X, apoptosis regulator Homo sapiens 188-191 22159556-11 2012 Emodin monotherapy or combination with gemcitabine both decreased the gene and protein expression levels of MDR-1 (P-gp), NF-kappaB and Bcl-2 and inhibited the function of P-gp, but increased the expression levels of Bax, cytochrome-C (cytosol), caspase-9 and -3, and promoted cell apoptosis. gemcitabine 39-50 BCL2 associated X, apoptosis regulator Homo sapiens 217-220 21570961-5 2011 When cells were treated with the combination of gemcitabine and ICI 118551, NF-kappaB activation was blocked; the expression of Bax protein was substantially increased; and Bcl-2 protein was downregulated. gemcitabine 48-59 BCL2 associated X, apoptosis regulator Homo sapiens 128-131 21305255-7 2011 Taken together, our results suggest that emodin improved the anti-tumor effect of gemcitabine, even at a lower dose of gemcitabine which could decrease the toxicity of chemotherapy, on transplanted tumors of the SW1990 cell line through the enhancement of apoptosis induced by gemcitabine, the mechanism of which may be through down-regulation of the Bcl-2/Bax ratio and promoting release of CytC from the mitochondria into the cytoplasm. gemcitabine 82-93 BCL2 associated X, apoptosis regulator Homo sapiens 357-360 20302733-6 2010 RESULTS: At 72 h after transfection, the combination with gemcitabine and p65 siRNA significantly decreased the cell viability index (P < 0.05), and down-regulated the expression of Bcl-2 and procaspase-3 and up-regulated the expression of Bax compared with other groups. gemcitabine 58-69 BCL2 associated X, apoptosis regulator Homo sapiens 243-246 19763526-3 2009 The present study demonstrates that treatment of glioma cells with clinically achievable doses of gemcitabine results in acid sphingomyelinase activation, lysosomal accumulation of ceramide, cathepsin D activation, Bax insertion into the mitochondria, and cell death. gemcitabine 98-109 BCL2 associated X, apoptosis regulator Homo sapiens 215-218 17984977-0 2008 Telomerase transcriptional targeting of inducible Bax/TRAIL gene therapy improves gemcitabine treatment of pancreatic cancer. gemcitabine 82-93 BCL2 associated X, apoptosis regulator Homo sapiens 50-53 17984977-3 2008 The present study explored the possibility of sensitizing pancreatic cancer to gemcitabine chemotherapy by combining the chemotherapy with the proapoptotic genes Bax and TNF-related apoptosis-inducing ligand (TRAIL). gemcitabine 79-90 BCL2 associated X, apoptosis regulator Homo sapiens 162-165 16162974-0 2005 Inhibition of phosphatidylinositol-3-kinase synergizes with gemcitabine in low-passage tumor cell lines correlating with Bax translocation to the mitochondria. gemcitabine 60-71 BCL2 associated X, apoptosis regulator Homo sapiens 121-124 16162974-6 2005 Finally, the analysis of the molecular markers that might be implicated in the synergism between LY294002 and gemcitabine suggests that PI3K inhibition might aid chemotherapeutic treatment, leading to changes in the balance between anti- and pro-apoptotic molecules of the Bcl-2 family, Bcl-XL and Bax. gemcitabine 110-121 BCL2 associated X, apoptosis regulator Homo sapiens 298-301 14750167-2 2004 We investigated the impact of anti-apoptotic Bcl-xL protein and its antagonist Bax on gemcitabine-induced apoptosis in human pancreatic carcinoma cells in vitro and in vivo. gemcitabine 86-97 BCL2 associated X, apoptosis regulator Homo sapiens 79-82 12138244-8 2002 The bax/bcl-2 ratio maintained relatively stable following 5-FU/gemcitabine treatment and reflected the chemotherapeutic sensitivity of these cell lines. gemcitabine 64-75 BCL2 associated X, apoptosis regulator Homo sapiens 4-7 10803919-5 2000 The cytotoxic effect of dFdCyd in RKO-P cells was accompanied by induction of the proapoptotic protein Bax at the time when p53 was induced. gemcitabine 24-30 BCL2 associated X, apoptosis regulator Homo sapiens 103-106 10803919-6 2000 In contrast, similar treatment of RKO-E6 cells with dFdCyd resulted in only limited expression of Bax, suggesting that the cytotoxic effect of dFdCyd was mediated, in part, by a p53-dependent apoptosis pathway. gemcitabine 52-58 BCL2 associated X, apoptosis regulator Homo sapiens 98-101 10341297-9 1999 Combination of auristatin-PE and gemcitabine showed significantly greater inhibition of cell growth and up-regulated expression of p21WAF1 and Bax. gemcitabine 33-44 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 34089613-8 2022 Gem + HY inhibits the expression of Bcl-2 but stimulates Bax level, triggering caspase activation and PARP cleavage and thus promoted apoptosis of Capan-2 cells. gemcitabine 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 57-60 33531986-9 2021 COL11A1/Akt disturbed the BCL-2/BAX balance, inhibiting cytochrome c (Cyt-C) release and binding of Apaf-1/procaspase-9/Cyt-C, which suppressed the apoptotic program and induced GEM resistance in pancreatic cancer cells. gemcitabine 178-181 BCL2 associated X, apoptosis regulator Homo sapiens 32-35 32599367-9 2020 FN2 in combination with GEM also decreased the level of Bcl-2 and increased the level of Bax. gemcitabine 24-27 BCL2 associated X, apoptosis regulator Homo sapiens 89-92 32522594-11 2021 When Bax was activated by BAM7 or Bcl-2 was inhibited by venetoclax, CCK-8 assays demonstrated that GEM sensitivity was restored in GEM-resistant cells. gemcitabine 100-103 BCL2 associated X, apoptosis regulator Homo sapiens 5-8 32522594-11 2021 When Bax was activated by BAM7 or Bcl-2 was inhibited by venetoclax, CCK-8 assays demonstrated that GEM sensitivity was restored in GEM-resistant cells. gemcitabine 132-135 BCL2 associated X, apoptosis regulator Homo sapiens 5-8 32522594-12 2021 When Bax was down-regulated by siRNA, CCK-8 assays verified that GEM sensitivity was decreased in PDAC cells. gemcitabine 65-68 BCL2 associated X, apoptosis regulator Homo sapiens 5-8 31521140-14 2019 Bax was upregulated while bcl-2, cIAP-2, and XIAP levels were downregulated in SW1990 and BxPC3 cells treated with gemcitabine and SN extracts. gemcitabine 115-126 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 30308458-6 2018 RESULTS: Incubation of PANC-1 cells with gemcitabine resulted in upregulation of pro-apoptotic bax and caspases proteins expression, downregulation of anti-apoptotic Bcl-2, heat shock proteins (HSPs) and modulation of cellular inhibitors of apoptosis (IAPs). gemcitabine 41-52 BCL2 associated X, apoptosis regulator Homo sapiens 95-98 30454541-14 2018 Furthermore, Western blot analysis showed that microwave hyperthermia combined with gemcitabine could up-regulate the p53, Caspase-3, Cleaved-Caspase-3, Cleaved-PARP and Bax protein expression. gemcitabine 84-95 BCL2 associated X, apoptosis regulator Homo sapiens 170-173