PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16749867-9 2006 HPMA copolymer-bound doxorubicin induced a time-dependent decrease in the expression of the anti-apoptotic Bcl-2 and Bcl-xL proteins, which control cell survival. Doxorubicin 21-32 BCL2 like 1 Homo sapiens 117-123 11236942-8 2001 Doxorubicin and melphalan were able to suppress bcl-XL expression only in the presence of IL-6. Doxorubicin 0-11 BCL2 like 1 Homo sapiens 48-54 16483679-6 2006 The combined treatment of TNF-alpha/DOX also resulted in a significant decrease of mRNA levels of anti-apoptotic genes, such as the cellular inhibitor of apoptosis-1 (c-IAP1), and the long isoform of B cell leukemia/lymphoma x gene (Bcl-xL), leading to efficient induction of caspase-8 cleavage and cell death. Doxorubicin 36-39 BCL2 like 1 Homo sapiens 233-239 11506966-4 2001 The protection was dose- and time-dependent -- maximal protection requiring pre-incubation with 100 ng/ml HGF for 48 h. Western blotting analysis and flow cytometric studies revealed that HGF inhibited doxorubicin- and etoposide-induced decreases in the levels of the anti-apoptotic proteins Bcl-X(L), and to a lesser extent Bcl-2, without inducing changes in the pro-apoptotic Bax protein. Doxorubicin 202-213 BCL2 like 1 Homo sapiens 292-300 11313718-3 2001 Bcl-x(L) overexpression did not affect sphingosine generation whereas it reduced apoptosis triggered by doxorubicin and completely blocked apoptosis triggered by sphingosine. Doxorubicin 104-115 BCL2 like 1 Homo sapiens 0-8 15893350-10 2005 On the other hand, the level of Bcl-xL transcripts at 24h incubation in FT-1 stimulated by doxorubicin and prednisolone were significantly increased about 4.2- and 5.8-folds to the controls and inducible level of Bcl-xL by vincristine was decreased about 0.35-folds. Doxorubicin 91-102 BCL2 like 1 Homo sapiens 32-38 15893350-10 2005 On the other hand, the level of Bcl-xL transcripts at 24h incubation in FT-1 stimulated by doxorubicin and prednisolone were significantly increased about 4.2- and 5.8-folds to the controls and inducible level of Bcl-xL by vincristine was decreased about 0.35-folds. Doxorubicin 91-102 BCL2 like 1 Homo sapiens 213-219 15911101-11 2005 However, the combinations attenuated also certain other influences on mRNA expression of the single agents, like, for example, the increases in Bcl-X(s) given by curcumin and doxorubicin. Doxorubicin 175-186 BCL2 like 1 Homo sapiens 144-149 15781649-8 2005 The knockdown of the predominant Bcl-XL overexpression significantly reduces the viability of pancreatic cancer cells to TNFalpha- and TRAIL-mediated apoptosis by sublethal-dose single and combined antitumor drugs, including geldanamycin, PS-341, Trichostatin A, and doxorubicine. Doxorubicin 267-279 BCL2 like 1 Homo sapiens 33-39 16280040-8 2005 Treatment of MDA-MB-231, BT-474, and ZR-75-1 cells with AS Bcl-xL increased chemosensitivity to DOX, MMC and taxanes to a smaller extent than AS Bcl-2. Doxorubicin 96-99 BCL2 like 1 Homo sapiens 59-65 12452453-0 2002 Bcl-2/bcl-xL bispecific antisense treatment sensitizes breast carcinoma cells to doxorubicin, paclitaxel and cyclophosphamide. Doxorubicin 81-92 BCL2 like 1 Homo sapiens 6-12 10381639-6 1999 In addition, overexpression of Bcl-XL in CEM cells blocked doxorubicin-triggered ROS and CD95-L expression. Doxorubicin 59-70 BCL2 like 1 Homo sapiens 31-37 11108797-0 2000 Down-regulation of bcr-abl and bcl-x(L) expression in a leukemia cell line and its doxorubicin-resistant variant by topoisomerase II inhibitors. Doxorubicin 83-94 BCL2 like 1 Homo sapiens 31-39 9642215-5 1998 Other cells selected for resistance to doxorubicin or vincristine also exhibited overexpression of Bcl-xL and failed to respond to CDDP and ara-C with activation of caspase-3. Doxorubicin 39-50 BCL2 like 1 Homo sapiens 99-105 9766678-2 1998 We investigated the sequence of these events in SHEP neuroblastoma cells transfected with Bcl-2 or Bcl-X(L) using two different drugs, namely, doxorubicin (Doxo), which activates the CD95/CD95 ligand (CD95-L) system, and betulinic acid (Bet A), which does not enhance the expression of CD95 or CD95-L and which, as shown here, directly targets mitochondria. Doxorubicin 143-154 BCL2 like 1 Homo sapiens 99-107 9766678-2 1998 We investigated the sequence of these events in SHEP neuroblastoma cells transfected with Bcl-2 or Bcl-X(L) using two different drugs, namely, doxorubicin (Doxo), which activates the CD95/CD95 ligand (CD95-L) system, and betulinic acid (Bet A), which does not enhance the expression of CD95 or CD95-L and which, as shown here, directly targets mitochondria. Doxorubicin 156-160 BCL2 like 1 Homo sapiens 99-107 7669718-6 1995 Another myeloid leukemia that shows barely detectable expression of bcl-2 also showed up-regulated expression of bcl-XL but no change in bax after induction of differentiation with granulocyte-macrophage colony-stimulating factor, and this reduced cell susceptibility to induction of apoptosis by Adriamycin or cycloheximide. Doxorubicin 297-307 BCL2 like 1 Homo sapiens 113-119 9443402-6 1998 BCL-X expression in malignant plasma cells strongly correlated with decreased response rates in patient groups treated with either melphalan and prednisone or vincristine, Adriamycin, and dexamethasone. Doxorubicin 172-182 BCL2 like 1 Homo sapiens 0-5 35526324-8 2022 DOX treatment promoted Beclin1 binding to Bcl-xL, disrupted mitophagy, and increased ROS accumulation in AC16 cells. Doxorubicin 0-3 BCL2 like 1 Homo sapiens 42-48 34608124-4 2021 The expressions of Bcl2 family members such as Bcl2, Bcl-xl, and Puma could be seen in U2OS and MG63 cells with or without doxorubicin, bortezomib, or paclitaxel treatment. Doxorubicin 123-134 BCL2 like 1 Homo sapiens 53-59 34190523-6 2021 RESULTS: Apigenin and doxorubicin dose-dependently inhibited cell survival, and co-administration of both agents significantly induced cell death via upregulating the mRNA expression of caspases, Bax and cytochrome c, and downregulating Bcl-XL. Doxorubicin 22-33 BCL2 like 1 Homo sapiens 237-243 35216449-8 2022 Conversely, Dox-induced CD133 expression diminished apoptosis in both trametinib-treated cell lines, coincident with elevated p-AKT, p-BAD, BCL-2, and BCL-xL and decreased activation of BAX and caspases-3 and -9. Doxorubicin 12-15 BCL2 like 1 Homo sapiens 151-157 35014203-6 2022 We found that the combination therapy of trastuzumab and doxorubicin may affect mitochondrial dysfunction in cardiomyocytes through different molecular pathways such as BCL-X and PGC-1alpha proteins, leading to a synergistic effect of cardiotoxicity. Doxorubicin 57-68 BCL2 like 1 Homo sapiens 169-174 32396934-8 2020 Increased expression of BCL-XL and/or CK2, as well as reduced IKAROS expression, are associated with resistance to doxorubicin treatment. Doxorubicin 115-126 BCL2 like 1 Homo sapiens 24-30 32801295-5 2020 Indeed, we found that BH3 mimetics that selectively target anti-apoptotic BCL-xL and MCL-1, synergistically enhance the effect of clinically used chemotherapeutic agents vincristine and doxorubicin in RMS cells. Doxorubicin 186-197 BCL2 like 1 Homo sapiens 74-80 32944866-7 2021 Further real-time PCR investigation displayed the expression of Bcl-xl, KI-67, TPX2 and BAX genes were significantly increased or decreased as desired in the cancer cell lines studied by treatment with doxorubicin or 2-azetidinone-anthraquinone 4gh. Doxorubicin 202-213 BCL2 like 1 Homo sapiens 64-70 30417787-3 2018 OBJECTIVE: The purpose of this study was to assess the molecular effects of doxorubicin (a 14-OH derivative of the natural product daunorubicin) and common chemotherapeutic drugs (used in the clinical practice to treat CRC) on the expression of the most prominent members of the BCL2 family, namely BCL2, BAX, BCLX, and MCL1. Doxorubicin 76-87 BCL2 like 1 Homo sapiens 310-314 29329420-0 2018 Pyrrolidine dithiocarbamate reverses Bcl-xL-mediated apoptotic resistance to doxorubicin by inducing paraptosis. Doxorubicin 77-88 BCL2 like 1 Homo sapiens 37-43 29329420-1 2018 Elevated Bcl-xL expression in cancer cells contributes to doxorubicin (DOX) resistance, leading to failure in chemotherapy. Doxorubicin 58-69 BCL2 like 1 Homo sapiens 9-15 29329420-1 2018 Elevated Bcl-xL expression in cancer cells contributes to doxorubicin (DOX) resistance, leading to failure in chemotherapy. Doxorubicin 71-74 BCL2 like 1 Homo sapiens 9-15 29329420-3 2018 Here, we show that co-treatment with pyrrolidine dithiocarbamate (PDTC) attenuates DOX-induced apoptosis in Chang-L liver cells and human hepatocytes, but overcomes DOX resistance in Bcl-xL-overexpressing Chang-L cells and several hepatocellular carcinoma (HCC) cell lines with high Bcl-xL expression. Doxorubicin 83-86 BCL2 like 1 Homo sapiens 283-289 29329420-3 2018 Here, we show that co-treatment with pyrrolidine dithiocarbamate (PDTC) attenuates DOX-induced apoptosis in Chang-L liver cells and human hepatocytes, but overcomes DOX resistance in Bcl-xL-overexpressing Chang-L cells and several hepatocellular carcinoma (HCC) cell lines with high Bcl-xL expression. Doxorubicin 165-168 BCL2 like 1 Homo sapiens 183-189 29329420-5 2018 These results suggest that DOX/PDTC co-treatment may provide a safe and effective therapeutic strategy against malignant hepatoma cells with Bcl-xL-mediated apoptotic defects. Doxorubicin 27-30 BCL2 like 1 Homo sapiens 141-147 29329420-7 2018 The intracellular glutathione levels were reduced in Bcl-xL-overexpressing Chang-L cells treated with DOX/PDTC, and DOX/PDTC-induced paraptosis was effectively blocked by pretreatment with thiol-antioxidants, but not by non-thiol antioxidants. Doxorubicin 102-105 BCL2 like 1 Homo sapiens 53-59 29329420-7 2018 The intracellular glutathione levels were reduced in Bcl-xL-overexpressing Chang-L cells treated with DOX/PDTC, and DOX/PDTC-induced paraptosis was effectively blocked by pretreatment with thiol-antioxidants, but not by non-thiol antioxidants. Doxorubicin 116-119 BCL2 like 1 Homo sapiens 53-59 29329420-8 2018 Collectively, our results suggest that disruption of thiol homeostasis may critically contribute to DOX/PDTC-induced paraptosis in Bcl-xL-overexpressing cells. Doxorubicin 100-103 BCL2 like 1 Homo sapiens 131-137 32340377-4 2020 Cell death caused by ATG/DOX co-treatment was mediated by the nuclear translocation of apoptosis inducing factor (AIF), reductions in cellular and mitochondrial Bcl-2 and Bcl-xL, and increases in mitochondrial BAX levels. Doxorubicin 25-28 BCL2 like 1 Homo sapiens 171-177 28947136-2 2018 Here, we report that BH3 mimetics selectively targeting BCL-xL, BCL-2 or MCL-1 (i.e. A-1331852, ABT-199, A-1210477) act in concert with multiple chemotherapeutic agents (i.e. vincristine (VCR), etoposide (ETO), doxorubicin, actinomycin D and cyclophosphamide) to induce apoptosis in rhabdomyosarcoma (RMS) cells. Doxorubicin 211-222 BCL2 like 1 Homo sapiens 56-62 28711493-7 2017 Sequential therapy with doxorubicin did not affect the replication of ZD55-shMYCN in doxorubicin-resistant neuroblastoma cells, but decreased the expression of Bcl-2, Bcl-XL, MMP-1. Doxorubicin 24-35 BCL2 like 1 Homo sapiens 167-173 28732245-6 2017 IL-4R-targeted BPEI-SPION/Bcl-xL siRNA more efficiently reduced Bcl-xL gene expression and enhanced cytotoxicity of doxorubicin in MDA-MB231 breast tumor cells compared to untargeted BPEI-SPION/Bcl-xL siRNA. Doxorubicin 116-127 BCL2 like 1 Homo sapiens 26-32 28236188-3 2017 In this study, alkyl-modified polyethylenimine (PEI 10 kD) was used for co-delivery of doxorubicin (DOX) encapsulated into poly lactic-co-glycolic acid (PLGA) nanoparticles (NPs) and Bcl-xL shRNA (one class of molecules that block apoptosis of tumor cells) into breast cancer cells. Doxorubicin 87-98 BCL2 like 1 Homo sapiens 183-189 28236188-3 2017 In this study, alkyl-modified polyethylenimine (PEI 10 kD) was used for co-delivery of doxorubicin (DOX) encapsulated into poly lactic-co-glycolic acid (PLGA) nanoparticles (NPs) and Bcl-xL shRNA (one class of molecules that block apoptosis of tumor cells) into breast cancer cells. Doxorubicin 100-103 BCL2 like 1 Homo sapiens 183-189 28230534-11 2017 In conclusion, silencing antiapoptotic genes such as BCL-2 and BCL-xL through the use of siRNA carried by hybrid nanoparticles showed to be effective in vitro, and presents a promising strategy for pre-clinical analysis, especially when combined with DOX against breast cancer. Doxorubicin 251-254 BCL2 like 1 Homo sapiens 63-69 28714472-6 2017 As doxorubicin and dinaciclib also reduced BCL-XL, the combinations of BCL-2 inhibitor ABT-199 (venetoclax) with doxorubicin or dinaciclib provided effective therapeutic strategies for SCLC. Doxorubicin 3-14 BCL2 like 1 Homo sapiens 43-49 27841296-7 2016 In HT-29 cells, the expression of Bcl-XL gene was significantly decreased after exposure to DOX/DID. Doxorubicin 92-95 BCL2 like 1 Homo sapiens 34-40 25818183-8 2015 Conversely after exposure to doxorubicin, these cells displayed an up-regulation of the anti-apoptotic proteins Bcl-2 and Bcl-xL with concomitant down-regulation of Bak and decreased caspase 3/7 activity. Doxorubicin 29-40 BCL2 like 1 Homo sapiens 122-128 26473375-4 2015 Mechanistically, JNJ-26481585/Doxorubicin cotreatment causes upregulation of the BH3-only proteins Bim and Noxa as well as downregulation of the antiapoptotic proteins Mcl-1 and Bcl-xL. Doxorubicin 30-41 BCL2 like 1 Homo sapiens 178-184 27222034-0 2016 MicroRNA-184 Modulates Doxorubicin Resistance in Osteosarcoma Cells by Targeting BCL2L1. Doxorubicin 23-34 BCL2 like 1 Homo sapiens 81-87 27222034-12 2016 Furthermore, doxorubicin reduced BCL2L1 expression, which was reversed by miR-184 overexpression and further decreased by miR-184 inhibition in OS cells. Doxorubicin 13-24 BCL2 like 1 Homo sapiens 33-39 27222034-14 2016 CONCLUSIONS Our data show that miR-184 was up-regulated in OS patients treated with doxorubicin therapy and leads to poor response to drug therapy by targeting BCL2L1. Doxorubicin 84-95 BCL2 like 1 Homo sapiens 160-166 26892009-5 2016 This study demonstrates that combination of doxorubicin and sorafenib induces apoptosis in MPNST cells through downregulation of B cell lymphoma protein 2 (Bcl-2), Bcl-2-related protein long form of Bcl-x (Bcl-xl), and myeloid cell leukemia 1 (Mcl-1). Doxorubicin 44-55 BCL2 like 1 Homo sapiens 199-204 26892009-5 2016 This study demonstrates that combination of doxorubicin and sorafenib induces apoptosis in MPNST cells through downregulation of B cell lymphoma protein 2 (Bcl-2), Bcl-2-related protein long form of Bcl-x (Bcl-xl), and myeloid cell leukemia 1 (Mcl-1). Doxorubicin 44-55 BCL2 like 1 Homo sapiens 206-212 26694174-0 2016 Bim directly antagonizes Bcl-xl in doxorubicin-induced prostate cancer cell apoptosis independently of p53. Doxorubicin 35-46 BCL2 like 1 Homo sapiens 25-31 26694174-8 2016 We further demonstrated that Bcl-xl protects LNCaP and PC3 cells from doxorubicin-induced apoptosis by using ABT-263, an inhibitor of Bcl-xl, as a single agent or in combination with doxorubicin to treat LNCaP or PC3 cells. Doxorubicin 70-81 BCL2 like 1 Homo sapiens 29-35 26694174-8 2016 We further demonstrated that Bcl-xl protects LNCaP and PC3 cells from doxorubicin-induced apoptosis by using ABT-263, an inhibitor of Bcl-xl, as a single agent or in combination with doxorubicin to treat LNCaP or PC3 cells. Doxorubicin 183-194 BCL2 like 1 Homo sapiens 29-35 26694174-9 2016 Bcl-xl rather than p53, likely contributes to the differential response of LNCaP and PC3 to doxorubicin in apoptosis. Doxorubicin 92-103 BCL2 like 1 Homo sapiens 0-6 26694174-10 2016 Finally, co-immunoprecipitation and siRNA analysis revealed that a BH3-only protein, Bim, is involved in doxorubicin-induced apoptosis by directly counteracting Bcl-xl. Doxorubicin 105-116 BCL2 like 1 Homo sapiens 161-167 26320837-7 2015 On the other hand, a sub-therapeutic DOX concentration (40 nM) results in highly altered c-fos, bcl-xl, and CLU transcript levels, and this is not affected by co-exposure with BPA. Doxorubicin 37-40 BCL2 like 1 Homo sapiens 96-102 26416351-0 2015 Pharmacological inhibition of Bcl-xL sensitizes osteosarcoma to doxorubicin. Doxorubicin 64-75 BCL2 like 1 Homo sapiens 30-36 26416351-8 2015 Nevertheless, pharmacological inhibition of a range of Bcl-2 family members showed that inhibitors targeting Bcl-xL synergistically enhanced the response to the chemotherapeutic agent, doxorubicin. Doxorubicin 185-196 BCL2 like 1 Homo sapiens 109-115 26416351-9 2015 Indeed, in osteosarcoma cells strongly expressing Bcl-xL, the Bcl-xL-selective BH3 mimetic, WEHI-539 potently enhanced apoptosis in the presence of low doses of doxorubicin. Doxorubicin 161-172 BCL2 like 1 Homo sapiens 50-56 26416351-9 2015 Indeed, in osteosarcoma cells strongly expressing Bcl-xL, the Bcl-xL-selective BH3 mimetic, WEHI-539 potently enhanced apoptosis in the presence of low doses of doxorubicin. Doxorubicin 161-172 BCL2 like 1 Homo sapiens 62-68 26504757-0 2015 Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells. Doxorubicin 0-11 BCL2 like 1 Homo sapiens 25-31 26504757-3 2015 The present study describes Bax, Bcl-xL gene expression and Caspase-8 and 9 protein levels in MCF-7 cells incubated with doxorubicin at different doses an incubation times. Doxorubicin 121-132 BCL2 like 1 Homo sapiens 33-39 26504757-5 2015 MCF-7 cells were treated with three concentrations of doxorubicin (0.1, 0.5, 1 muM) and incubated for 24, 48 and 72 hours then expression levels of Bax and Bcl-xL genes were elucidated by Real-time RT-PCR technique and protein levels of caspase-8 and caspase-9 proteins were measured using ELISA method. Doxorubicin 54-65 BCL2 like 1 Homo sapiens 156-162 26504757-7 2015 RESULTS: Doxorubicin decreased the anti-apoptotic Bcl-xL and increased pro-apoptotic Bax mRNA levels. Doxorubicin 9-20 BCL2 like 1 Homo sapiens 50-56 26504757-8 2015 Doxorubicin induced a significant increase in Bax /Bcl-xL ratio in all doses and incubation times (p<0.05). Doxorubicin 0-11 BCL2 like 1 Homo sapiens 51-57 26504757-9 2015 Highest (more than 10 fold) increase in Bax /Bcl-xL ratio was revealed after 48 h incubation of the cells with in all doses of doxorubicin. Doxorubicin 127-138 BCL2 like 1 Homo sapiens 45-51 26504757-11 2015 CONCLUSION: Our results confirm that doxorubicin induces mitochondrial-dependent apoptosis by down-regulation of Bcl-xL and up- regulation of Bax and caspase-9 expressions. Doxorubicin 37-48 BCL2 like 1 Homo sapiens 113-119 25789066-0 2015 A let-7b binding site SNP in the 3"-UTR of the Bcl-xL gene enhances resistance to 5-fluorouracil and doxorubicin in breast cancer cells. Doxorubicin 101-112 BCL2 like 1 Homo sapiens 47-53 25789066-4 2015 The data indicated that let-7b negatively regulates the expression of Bcl-xL and appears to sensitize MCF-7 cells to the chemotherapeutic agents 5-fluorouracil (5-FU) and doxorubicin. Doxorubicin 171-182 BCL2 like 1 Homo sapiens 70-76 25789066-5 2015 Furthermore, the SNP rs3208684 A>C was demonstrated to enhance Bcl-xL protein expression by disrupting the binding of let-7b to the 3"-UTR of Bcl-xL and, in MCF-7 cells, overexpression of let-7b in the presence of a mutant Bcl-xL 3"-UTR (C allele) significantly increased 5-FU and doxorubicin resistance. Doxorubicin 284-295 BCL2 like 1 Homo sapiens 66-72 25789066-6 2015 Thus, the results of the present study demonstrate that the SNP rs3208684 A>C may upregulate Bcl-xL protein expression and enhance the resistance of the MCF-7 cells to 5-FU and doxorubicin by decreasing the binding of let-7b to the 3"-UTR of Bcl-xL. Doxorubicin 180-191 BCL2 like 1 Homo sapiens 96-102 25789066-6 2015 Thus, the results of the present study demonstrate that the SNP rs3208684 A>C may upregulate Bcl-xL protein expression and enhance the resistance of the MCF-7 cells to 5-FU and doxorubicin by decreasing the binding of let-7b to the 3"-UTR of Bcl-xL. Doxorubicin 180-191 BCL2 like 1 Homo sapiens 245-251 23965755-8 2013 Finally, we show that direct inhibition of Bcl-xL by small molecule antagonist ABT-737 sensitizes GBM cells to doxorubicin. Doxorubicin 111-122 BCL2 like 1 Homo sapiens 43-49 24626197-7 2014 The micro-opioid receptor agonist D,L-methadone sensitizes glioblastoma as well as the untreatable glioblastoma stem cells for doxorubicin-induced apoptosis and activation of apoptosis pathways by reversing deficient caspase activation and deficient downregulation of XIAP and Bcl-xL, playing critical roles in glioblastomas" resistance. Doxorubicin 127-138 BCL2 like 1 Homo sapiens 277-283 25243873-11 2015 Citral (40 microM) in combination with doxorubicin (1.5 microM) increased the expression of pro-apoptotic protein BAK but significantly decreased the expression of anti-apoptotic protein BCL-XL to 5.26-fold compared with doxorubicin-treated cells. Doxorubicin 39-50 BCL2 like 1 Homo sapiens 187-193 24814395-6 2014 Also, cotreatment with SAHA and Doxorubicin changes the ratio of pro- and antiapoptotic Bcl-2 proteins with downregulation of Mcl-1 and Bcl-xL, dephosphorylation of Bcl-2 and upregulation of BimEL, thus shifting the balance towards apoptosis. Doxorubicin 32-43 BCL2 like 1 Homo sapiens 136-142 23613425-2 2013 In this study, Bcl-xL siRNA and doxorubicin (DOX) are encapsulated into designed methoxy-poly(ethylene glycol)-block-poly(D,L-lactic acid) (mPEG-b-PLA) block copolymer polymersomes (PSomes). Doxorubicin 45-48 BCL2 like 1 Homo sapiens 15-21 21357440-5 2011 Doxorubicin or bortezomib combined with TRA-8 also reduced Bcl-XL and X-linked inhibitors of apoptosis (XIAP) in treated cells. Doxorubicin 0-11 BCL2 like 1 Homo sapiens 59-65 23292448-4 2013 We also discovered that the increased Bcl-xL expression caused an increase in drug resistance to doxorubicin in MPNST-derived SCs. Doxorubicin 97-108 BCL2 like 1 Homo sapiens 38-44 23292448-7 2013 As the reduction of Bcl-xL expression restored sensitivity to doxorubicin-induced apoptosis in sNF96.2 cells, we examined the effect of the small molecule Bcl-xL inhibitor ABT-737 on sNF96.2 cells. Doxorubicin 62-73 BCL2 like 1 Homo sapiens 20-26 23232767-6 2013 Western blotting revealed that, following exposure to doxorubicin, YAP-overexpressing cells exhibited decreased cleaved PARP, increased phosphorylation of Akt and ERK1/2, and elevated Bcl-xL expression in comparison to the vector control. Doxorubicin 54-65 BCL2 like 1 Homo sapiens 208-214 22664653-7 2012 We further demonstrated that either depletion of Bcl-xL expression by RNAi or inactivation of Bcl-xL by ABT-737, a mimetic of the BH3-only protein BAD, was very effective in sensitizing the MPNST cells to apoptotic cell death by combined treatment with the tested anticancer drug doxorubicin. Doxorubicin 316-327 BCL2 like 1 Homo sapiens 61-67 22664653-7 2012 We further demonstrated that either depletion of Bcl-xL expression by RNAi or inactivation of Bcl-xL by ABT-737, a mimetic of the BH3-only protein BAD, was very effective in sensitizing the MPNST cells to apoptotic cell death by combined treatment with the tested anticancer drug doxorubicin. Doxorubicin 316-327 BCL2 like 1 Homo sapiens 106-112 21763329-13 2011 CASP9 expression was increased and BCL-XL expression decreased in the selenium (500ng/mL) and doxorubicin group. Doxorubicin 94-105 BCL2 like 1 Homo sapiens 35-41 20206622-11 2010 Bcl-2 and Bcl-X(L) but not p53 may contribute to doxorubicin-induced apoptosis through Etk pathway. Doxorubicin 49-60 BCL2 like 1 Homo sapiens 10-18 20811701-7 2010 Cell surface stimulation of TLR9 promoted cell proliferation, and, furthermore, the TLR9 agonists, CpG-ODNs, reduced the cytotoxicity of the anti-cancer drug adriamycin (ADM) via up-regulation of apoptosis inhibitors such as survivin, Bcl-xL, XIAP and cFLIP, in HCC cell lines. Doxorubicin 158-168 BCL2 like 1 Homo sapiens 235-241 20400521-6 2010 RESULTS: BLID was found to interact with Bcl-X(L), and the binding was enhanced in cancer cells exposed to doxorubicin or cisplatin. Doxorubicin 107-118 BCL2 like 1 Homo sapiens 41-49 20206622-6 2010 Furthermore, the levels of Bcl-2 and Bcl-X(L) significantly increased in H446-Etk cells than that in H446 cells after doxorubicin treatment, and were positively associated with Etk expression. Doxorubicin 118-129 BCL2 like 1 Homo sapiens 37-45 20884855-3 2010 Cotreatment with sildenafil enhanced DOX-induced apoptosis in PC-3 and DU145 prostate cancer cells, which was mediated by enhanced generation of reactive oxygen species, up-regulation of caspase-3 and caspase-9 activities, reduced expression of Bcl-xL, and phosphorylation of Bad. Doxorubicin 37-40 BCL2 like 1 Homo sapiens 245-251 20884855-4 2010 Overexpression of Bcl-xL or dominant negative caspase 9 attenuated the synergistic effect of sildenafil and DOX on prostate cancer cell killing. Doxorubicin 108-111 BCL2 like 1 Homo sapiens 18-24 20820630-8 2010 In particular, examination of drug/gene interactions on collections of 3D hepatoma mu-tissues indicated synergistic influence of doxorubicin and siRNA knockdown of the anti-apoptotic gene BCL-XL. Doxorubicin 129-140 BCL2 like 1 Homo sapiens 188-194 16843435-7 2006 In addition to the impact on Bad phosphorylation, doxorubicin-treatment caused p38 MAPK-dependent downregulation of Bcl-xL protein. Doxorubicin 50-61 BCL2 like 1 Homo sapiens 116-122 19502069-0 2009 Interaction of doxorubicin with the subcellular structures of the sensitive and Bcl-xL-overexpressing MCF-7 cell line: confocal and low-energy-loss transmission electron microscopy. Doxorubicin 15-26 BCL2 like 1 Homo sapiens 80-86 19502069-1 2009 The present investigation was directed to examine the interaction of the anti-cancer agent doxorubicin (DOX) with the subcellular compartments of the drug sensitive and Bcl-xL-overexpressing (Bcl-xL) MCF-7 cells using confocal and low-energy-loss transmission electron microscopy (LELTEM). Doxorubicin 91-102 BCL2 like 1 Homo sapiens 169-190 19502069-1 2009 The present investigation was directed to examine the interaction of the anti-cancer agent doxorubicin (DOX) with the subcellular compartments of the drug sensitive and Bcl-xL-overexpressing (Bcl-xL) MCF-7 cells using confocal and low-energy-loss transmission electron microscopy (LELTEM). Doxorubicin 91-102 BCL2 like 1 Homo sapiens 169-175 19502069-1 2009 The present investigation was directed to examine the interaction of the anti-cancer agent doxorubicin (DOX) with the subcellular compartments of the drug sensitive and Bcl-xL-overexpressing (Bcl-xL) MCF-7 cells using confocal and low-energy-loss transmission electron microscopy (LELTEM). Doxorubicin 104-107 BCL2 like 1 Homo sapiens 169-190 19502069-1 2009 The present investigation was directed to examine the interaction of the anti-cancer agent doxorubicin (DOX) with the subcellular compartments of the drug sensitive and Bcl-xL-overexpressing (Bcl-xL) MCF-7 cells using confocal and low-energy-loss transmission electron microscopy (LELTEM). Doxorubicin 104-107 BCL2 like 1 Homo sapiens 169-175 19502069-5 2009 When the sensitive and Bcl-xL cells were examined under the confocal microscope after 1 min, DOX uptake could not be detected in the nuclei nor in the cytoplasm whereas LELTEM observation revealed that at this stage of incubation the drug has already been incorporated by both cell types and that the nuclear membrane, nucleolus, and mitochondria of the Bcl-xL cells were temporally less DOX-responsive as compared to the sensitive cells. Doxorubicin 93-96 BCL2 like 1 Homo sapiens 23-29 19082486-4 2009 Doxorubicin induced dose-dependent G2/M and/or G1/S cell cycle arrest, followed by grade- and dose-dependent reduction in the amount of the cytosolic trimeric form of FasL, activation of Caspase-8, Caspase-9, Caspase-3, cleavage of PARP, Lamin A/C, Bcl-XL/S and interestingly Hsp90, and finally cell death. Doxorubicin 0-11 BCL2 like 1 Homo sapiens 249-257 17922852-8 2007 Furthermore, the combination of doxorubicin and lexatumumab significantly enhanced caspase 8 activity, Bid cleavage, Bcl-xL decrease, release of cytochrome c, and caspase 9 and caspase 3 activity, and induced synergistic apoptosis. Doxorubicin 32-43 BCL2 like 1 Homo sapiens 117-123 17923112-0 2007 Bcl-xL blocks high dose doxorubicin-induced apoptosis but not low dose doxorubicin-induced cell death through mitotic catastrophe. Doxorubicin 24-35 BCL2 like 1 Homo sapiens 0-6 17923112-2 2007 In this study, we investigated the role of Bcl-xL in two modes of cell death induced by different doses of doxorubicin, apoptosis and cell death through mitotic catastrophe. Doxorubicin 107-118 BCL2 like 1 Homo sapiens 43-49 17923112-3 2007 Bcl-xL overexpression in various hepatoma cells effectively blocked apoptosis induced by high dose doxorubicin, inhibiting the loss of mitochondrial membrane potential, release of mitochondrial cytochrome c and caspase activation. Doxorubicin 99-110 BCL2 like 1 Homo sapiens 0-6 17923112-5 2007 These findings indicate that low dose doxorubicin-induced cell death through mitotic catastrophe may provide an alternative therapeutic strategy for Bcl-xL-overexpressing hepatoma cells, which are resistant to pro-apoptotic treatments. Doxorubicin 38-49 BCL2 like 1 Homo sapiens 149-155 19502069-6 2009 As the incubation time increased, nuclear membranes and nucleoli of both cell types appeared equally sensitive to DOX, nonetheless, mitochondria of the Bcl-xL cells remained invulnerable to DOX for 24h. Doxorubicin 190-193 BCL2 like 1 Homo sapiens 152-158 19502069-7 2009 The results point to LELTEM feasibility to better characterize yet unresolved cellular events caused by DOX and suggest a transitory role for Bcl-xL overexpression in protecting the cellular compartments from DOX invasion. Doxorubicin 209-212 BCL2 like 1 Homo sapiens 142-148 19726787-4 2009 Overexpression of the antiapoptotic protein Bcl-XL, alone or in combination with the inhibitor Z-VAD-FMK, attenuated caspase activation in HeLa cells exposed to doxorubicin, etoposide, or cell death siRNA. Doxorubicin 161-172 BCL2 like 1 Homo sapiens 44-50 18560228-8 2008 However, the Bcl-x(L)level increased in sensitive cells after 72 h of doxorubicin incubation. Doxorubicin 70-81 BCL2 like 1 Homo sapiens 13-18 17912235-3 2008 By achieving selective, targeted, and early inhibition of NF-kappaB activity, we demonstrate that NF-kappaB plays a critical role in Dox-induced chemoresistance by regulating genes involved in proliferation (Ki-67), response to DNA damage (GADD153), antiapoptosis (Bcl-XL), and pH regulation (CA9). Doxorubicin 133-136 BCL2 like 1 Homo sapiens 265-271 17140381-0 2006 Changes in expression of genes encoding antioxidant enzymes, heme oxygenase-1, Bcl-2, and Bcl-xl and in level of reactive oxygen species in tumor cells resistant to doxorubicin. Doxorubicin 165-176 BCL2 like 1 Homo sapiens 90-96 16928273-11 2006 Finally in MCF-7 cells, Bcl-XL is approximately ten times more active than Bcl-2 in repressing apoptosis induced by doxorubicin. Doxorubicin 116-127 BCL2 like 1 Homo sapiens 24-30 16608847-4 2006 We found that Bcl-X(L) was most effective among several antiapoptotic proteins in suppressing PUMA-induced apoptosis and PUMA-dependent apoptosis induced by the DNA-damaging agent adriamycin. Doxorubicin 180-190 BCL2 like 1 Homo sapiens 14-22 16608847-7 2006 Furthermore, Bax was found to be dissociated preferentially from Bcl-X(L) in HCT116 cells but not in the PUMA-knockout cells, in response to PUMA induction and adriamycin treatment. Doxorubicin 160-170 BCL2 like 1 Homo sapiens 65-73