PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12553012-2 2002 Over-expression of Bcl-xl inhibits apoptotic changes induced by Etoposide including cytochrome-c release, caspase-3 activation and DNA fragmentation. Etoposide 64-73 BCL2 like 1 Homo sapiens 19-25 12553012-3 2002 However, Etoposide treatment resulted in cell death in U937 cells over-expressing Bcl-xl, which had a necrotic-like phenotype with no evidence of caspase-3 activation. Etoposide 9-18 BCL2 like 1 Homo sapiens 82-88 11929841-8 2002 The down-regulation of bcl-xL in both DU145 (and to a much lesser extent in LNCaP) cells led to their resistance to cytotoxic agents, including docetaxel, mitoxantrone, etoposide, vinblastine, and carboplatin. Etoposide 169-178 BCL2 like 1 Homo sapiens 23-29 11815602-0 2002 Fibroblast growth factor-2 induces translational regulation of Bcl-XL and Bcl-2 via a MEK-dependent pathway: correlation with resistance to etoposide-induced apoptosis. Etoposide 140-149 BCL2 like 1 Homo sapiens 63-69 11346470-5 2001 Treatment with etoposide increased expression of p53 and decreased expression of Bcl-X(L) in U-373MG cells which harbored mutant p53. Etoposide 15-24 BCL2 like 1 Homo sapiens 81-89 11431014-0 2001 Resistance of CD4-positive T lymphocytes to etoposide-induced apoptosis mediated by upregulation of Bcl-xL expression in patients with HTLV-I-associated myelopathy. Etoposide 44-53 BCL2 like 1 Homo sapiens 100-106 11260076-2 2001 We have tested the hypothesis that the susceptibility of Bcl-XL-expressing leukaemic cells to apoptosis induced by VP16 (etoposide) can be enhanced by pharmacological downregulation of Bcl-XL in vivo. Etoposide 115-119 BCL2 like 1 Homo sapiens 57-63 11260076-2 2001 We have tested the hypothesis that the susceptibility of Bcl-XL-expressing leukaemic cells to apoptosis induced by VP16 (etoposide) can be enhanced by pharmacological downregulation of Bcl-XL in vivo. Etoposide 115-119 BCL2 like 1 Homo sapiens 185-191 11260076-2 2001 We have tested the hypothesis that the susceptibility of Bcl-XL-expressing leukaemic cells to apoptosis induced by VP16 (etoposide) can be enhanced by pharmacological downregulation of Bcl-XL in vivo. Etoposide 121-130 BCL2 like 1 Homo sapiens 57-63 11260076-2 2001 We have tested the hypothesis that the susceptibility of Bcl-XL-expressing leukaemic cells to apoptosis induced by VP16 (etoposide) can be enhanced by pharmacological downregulation of Bcl-XL in vivo. Etoposide 121-130 BCL2 like 1 Homo sapiens 185-191 10850456-9 2000 Tumor cells overexpressing Bcl-2 or Bcl-xL become resistant to apoptosis induced by the chemotherapeutic drug etoposide. Etoposide 110-119 BCL2 like 1 Homo sapiens 36-42 10918609-9 2000 In addition, transient overexpression of Bcl-xL also exerted inhibitory effects on ceramide formation and apoptotic cell death induced by etoposide. Etoposide 138-147 BCL2 like 1 Homo sapiens 41-47 10381626-2 1999 Exposure of undifferentiated U937 cells to 50 microM etoposide for 6 h, that triggers apoptosis in 80% cells, activates procaspase-2L, -3 and -8, induces the mitochondrial release of cytochrome c and decreases Mcl-1 expression without modifying Bcl-2, Bcl-xL and Bax protein levels. Etoposide 53-62 BCL2 like 1 Homo sapiens 252-258 10620629-0 2000 Epigenetic determinants of resistance to etoposide regulation of Bcl-X(L) and Bax by tumor microenvironmental factors. Etoposide 41-50 BCL2 like 1 Homo sapiens 65-73 10839193-7 2000 Changes of the mRNA levels of most apoptosis-regulating genes were not prominent at both concentrations, except for the rapid induction of c-IAP-2/HIAP-1 and the down-regulation of Bcl-X(L) by 100 microM etoposide. Etoposide 204-213 BCL2 like 1 Homo sapiens 181-188 10839193-8 2000 The downregulation of Bcl-X(L) protein occurred from 6 h, while Bax protein conversely showed a slight increase from 6 h. Taken together, the present findings show that the dose-dependent apoptotic effect of etoposide is based on a change in the balance between Bcl-X(L) and Bax, which precedes the activation of caspase-3. Etoposide 208-217 BCL2 like 1 Homo sapiens 22-30 10839193-8 2000 The downregulation of Bcl-X(L) protein occurred from 6 h, while Bax protein conversely showed a slight increase from 6 h. Taken together, the present findings show that the dose-dependent apoptotic effect of etoposide is based on a change in the balance between Bcl-X(L) and Bax, which precedes the activation of caspase-3. Etoposide 208-217 BCL2 like 1 Homo sapiens 262-270 10620629-10 2000 Activation of surface protein CD40 increased Bcl-x(L) protein levels via an (E)-capsaicin-inhibitable activation of NF-kappaB; i.e. , (E)-capsaicin restored etoposide sensitivity. Etoposide 157-166 BCL2 like 1 Homo sapiens 45-53 10620629-12 2000 VCAM-1- and interleukin 4-mediated signals diminished conformational changes in Bax protein and prevented the etoposide-induced disruption of constitutive Bax-Bcl-x(L) binding. Etoposide 110-119 BCL2 like 1 Homo sapiens 159-164 10620629-13 2000 CONCLUSIONS: Microenvironmental factors reduce the sensitivity of a B-cell lymphoma to etoposide in vitro by modulating the expression and functions of Bax and Bcl-x(L). Etoposide 87-96 BCL2 like 1 Homo sapiens 160-165 10050882-7 1999 Downregulation of Bcl-X(L) to the same extent using antisense oligonucleotides enhanced etoposide-induced apoptosis by twofold. Etoposide 88-97 BCL2 like 1 Homo sapiens 18-26 10732782-7 1999 Etoposide diminished the binding between Bax and Bcl-XL but this was restored by IL-4 and VCAM-1 triggered signals. Etoposide 0-9 BCL2 like 1 Homo sapiens 49-55 9699642-1 1998 Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function. Etoposide 54-63 BCL2 like 1 Homo sapiens 142-148 9699642-1 1998 Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function. Etoposide 54-63 BCL2 like 1 Homo sapiens 192-198 9699642-8 1998 Exposure to etoposide (50 microM) or ara-C (100 microM) for 4 h induced apoptosis in HL-60/neo cells, but not in HL-60/Bcl-2, HL-60/Bcl-xL, HL-60/Bcl-2delta, or HL-60/Bcl-xLdelta cells. Etoposide 12-21 BCL2 like 1 Homo sapiens 132-138 9570926-5 1998 Modulation of cell death by Bcl-xL was also observed in cells treated with etoposide, vinblastine, paclitaxel, and cisplatinum (II) diammine dichloride. Etoposide 75-84 BCL2 like 1 Homo sapiens 28-34 8663611-6 1996 Furthermore, overexpression of Bcl-xL blocked DNA fragmentation, CPP32 activation and cleavage of poly(ADP-ribose) polymerase in U937 cells treated with both PI 3-kinase inhibitors and etoposide, but not in cells treated with TNFalpha. Etoposide 185-194 BCL2 like 1 Homo sapiens 31-37 8840993-12 1996 High Bcl-2 and Bcl-xL levels in these cells also inhibited Yama protease activity, PARP degradation, and apoptosis due to clinically relevant concentrations of etoposide and mitoxantrone. Etoposide 160-169 BCL2 like 1 Homo sapiens 15-21 8798452-0 1996 Bax can antagonize Bcl-XL during etoposide and cisplatin-induced cell death independently of its heterodimerization with Bcl-XL. Etoposide 33-42 BCL2 like 1 Homo sapiens 19-25 9494534-9 1997 Expression of bcl-2 family members (bax, bcl-x) was modulated by fotemustine, etoposide and cisplatin. Etoposide 78-87 BCL2 like 1 Homo sapiens 41-46 7655019-4 1995 Bcl-XL expression dramatically reduces the cytotoxicity of bleomycin, cisplatin, etoposide, vincristine, hygromycin B, and mycophenolic acid for up to 4 days in culture. Etoposide 81-90 BCL2 like 1 Homo sapiens 0-6 18758060-1 2008 Here, we confirmed that stable expression of B-cell lymphoma-xL (Bcl-xL) in N18TG neuroglioma cells could suppress c-Jun N-terminal protein kinase (JNK) activation, nuclear fragmentation, and cell death caused by etoposide treatment. Etoposide 213-222 BCL2 like 1 Homo sapiens 45-63 34322387-11 2021 Conclusion: Downregulation of ATXN3 enhanced AKT inhibitors (perifosine or MK-2206) induced cell death by BIM, but decreased the cell death induced by chemotherapeutic drugs (etoposide or cisplatin) via Bcl-xl. Etoposide 175-184 BCL2 like 1 Homo sapiens 203-209 22072718-8 2011 Further studies showed that overexpression of INrf2 enhanced degradation of PGAM5-Bcl-xL complex, led to etoposide-mediated accumulation of Bax, increased release of cytochrome c from mitochondria, activated caspase-3/7, and enhanced DNA fragmentation and apoptosis. Etoposide 105-114 BCL2 like 1 Homo sapiens 82-88 34678222-11 2021 Etoposide exposure in DFF40 deficient cells induces higher mortality levels and downregulation of Bcl-xL cells compared to DFF40 expressing T cells. Etoposide 0-9 BCL2 like 1 Homo sapiens 98-104 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. Etoposide 194-203 BCL2 like 1 Homo sapiens 56-62 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. Etoposide 205-208 BCL2 like 1 Homo sapiens 56-62 22617334-3 2012 Analysis of the dynamic phosphorylation and location of phospho-Bcl-xL(Ser62) in unperturbed, synchronized cells and during DNA damage-induced G 2 arrest discloses that a pool of phospho-Bcl-xL(Ser62) accumulates into nucleolar structures in etoposide-exposed cells during G 2 arrest. Etoposide 242-251 BCL2 like 1 Homo sapiens 64-70 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. Etoposide 174-183 BCL2 like 1 Homo sapiens 44-50 19488402-10 2009 Similar to silencing of IKKbeta, increasing the level of Bcl-xL in neurons prevents etoposide-induced caspase activation and Htt proteolysis. Etoposide 84-93 BCL2 like 1 Homo sapiens 57-63 18758060-1 2008 Here, we confirmed that stable expression of B-cell lymphoma-xL (Bcl-xL) in N18TG neuroglioma cells could suppress c-Jun N-terminal protein kinase (JNK) activation, nuclear fragmentation, and cell death caused by etoposide treatment. Etoposide 213-222 BCL2 like 1 Homo sapiens 65-71 18071312-4 2008 Co-treatment, but not single treatment, with VP16 and TSA induced apoptosis in a caspase-dependent manner accompanied by a crucial decrease in Bcl-xL expression allowing Bax activation and subsequent initiation of the apoptosis inducing factor (AIF)-dependent death pathway. Etoposide 45-49 BCL2 like 1 Homo sapiens 143-149 15674333-3 2005 Here we show that three representative apoptotic stimuli, that is, serum starvation, a mitochondrial toxin, and a DNA-damaging agent (etoposide), rapidly induce several distinct classes of prosurvival molecules, in particular, Bcl-2/Bcl-X(L) and superoxide dismutase (SOD; including both MnSOD and Cu/ZnSOD). Etoposide 134-143 BCL2 like 1 Homo sapiens 233-241 16960866-5 2006 Both inhibitors and stable expression of SR-IkB are associated with down-modulation of the antiapoptotic protein Bcl-xL, suggesting that the survival pathway activated by Etoposide involves NF-kB-mediated Bcl-xL expression. Etoposide 171-180 BCL2 like 1 Homo sapiens 113-119 16960866-5 2006 Both inhibitors and stable expression of SR-IkB are associated with down-modulation of the antiapoptotic protein Bcl-xL, suggesting that the survival pathway activated by Etoposide involves NF-kB-mediated Bcl-xL expression. Etoposide 171-180 BCL2 like 1 Homo sapiens 205-211 15657350-9 2005 Additionally, (-)-gossypol was more efficient than etoposide at inducing caspase-3 activation and phosphatidylserine externalization in the setting of Bcl-2 or Bcl-X(L) overexpression. Etoposide 51-60 BCL2 like 1 Homo sapiens 160-168 14745596-11 2004 Bcl-XL was expressed endogenously in both cell lines and had reduced expression in EBV-negative cells after etoposide treatment. Etoposide 108-117 BCL2 like 1 Homo sapiens 0-6 12618199-8 2003 Regardless of the molecular mechanisms underlying the cell death, sequential treatment with etoposide and TRAIL could be useful in the design of treatment modalities for patients with SCC, especially those with elevated levels of Bcl-x(L). Etoposide 92-101 BCL2 like 1 Homo sapiens 230-238