PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15788689-7 2005 The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel. Etoposide 133-142 caspase 8 Homo sapiens 69-77 16442262-4 2006 To show conventional chemotherapy drugs can trigger the caspase cascade, including caspase-8, -9, -3 and DNA fragmentation factor, Jurkat T leukemia cells were treated with cisplatin or etoposide in a dose-dependent and a time-dependent manner. Etoposide 186-195 caspase 8 Homo sapiens 83-129 16319070-8 2006 When given with tumor necrosis factor-related apoptosis-inducing ligand or caspase-dependent chemotherapeutic agents, such as etoposide and paclitaxel, troglitazone exhibited a synergistic effect by facilitating caspase-8/9 activities. Etoposide 126-135 caspase 8 Homo sapiens 212-221 16722146-8 2006 Further, in Ca922 and HSC6 but not in HOC313, caspase 8 inhibitor restored loss of viability induced either with LY294002 and TRAIL or even with etoposide alone. Etoposide 145-154 caspase 8 Homo sapiens 46-55 15615731-6 2005 Finally, we show that the extensive caspase 8 cleavage seen during TRAIL-etoposide synergy is a consequence and not a cause of the apoptotic cascade activated downstream of Bid. Etoposide 73-82 caspase 8 Homo sapiens 36-45 16010441-13 2005 We also found that etoposide bypassed Fas-FADD interaction in MML-1R by activating caspase-8 and caspase-3. Etoposide 19-28 caspase 8 Homo sapiens 83-92 15161627-5 2004 The appearance of diminished FRET was inhibited by a pan-caspase inhibitor z-VAD or D->A mutations in the LEVD sequence and was markedly increased by apoptosis-inducing agents, etoposide and camptothecin, or overexpression of a caspase 8-red fluorescent protein fusion protein. Etoposide 180-189 caspase 8 Homo sapiens 231-240 15611097-6 2005 Using an in vivo affinity labeling approach, we demonstrate that caspase-8 is activated in etoposide-treated cells in vivo in the absence of the receptor-induced death-inducing signaling complex formation. Etoposide 91-100 caspase 8 Homo sapiens 65-74 15262979-0 2004 Sequential caspase-2 and caspase-8 activation upstream of mitochondria during ceramideand etoposide-induced apoptosis. Etoposide 90-99 caspase 8 Homo sapiens 25-34 15262979-9 2004 Similarly, sequential caspase-2 and caspase-8 activation upstream of mitochondria was also observed in etoposide-induced apoptosis. Etoposide 103-112 caspase 8 Homo sapiens 36-45 15262979-10 2004 These data suggest sequential initiator caspase-2 and caspase-8 activation in the mitochondrial apoptotic pathway induced by ceramide or etoposide. Etoposide 137-146 caspase 8 Homo sapiens 54-63 15454884-5 2004 Treatment of HUVECs with LLL-CHO, etoposide, or C2-ceramide induced DeltaPsim, activation of caspase-3, caspase-8, and caspase-9 and the appearance of hypodiploid DNA-positive cells. Etoposide 34-43 caspase 8 Homo sapiens 104-113 15254227-0 2004 Association of active caspase 8 with the mitochondrial membrane during apoptosis: potential roles in cleaving BAP31 and caspase 3 and mediating mitochondrion-endoplasmic reticulum cross talk in etoposide-induced cell death. Etoposide 194-203 caspase 8 Homo sapiens 22-31 15254227-4 2004 In MDA-MB231 breast cancer cells treated with etoposide (VP16), active caspase 8 is detected only in the membrane fraction, which contains both mitochondria and endoplasmic reticulum (ER), as revealed by fractionation studies. Etoposide 46-55 caspase 8 Homo sapiens 71-80 12605597-4 2003 Indeed, using Jurkat cells as a model system, we demonstrate that NO donors block Fas- and etoposide-induced caspase activation and apoptosis (downstream of mitochondrial membrane depolarization) and cytochrome c release. Etoposide 91-100 caspase 8 Homo sapiens 109-116 12881712-3 2003 FOXO3a was cleaved in vivo by caspases in leukemic Jurkat cells following engagement of Fas (CD95) receptor, staurosporine, and etoposide treatment, but not following engagement of CD99, a caspase-independent cell death inducer. Etoposide 128-137 caspase 8 Homo sapiens 30-38 14519653-5 2003 The remaining cell lines and primary cultures were resistant to TRAIL, but cisplatin, chemptothecin, and etoposide sensitized the resistant cell lines and primary cultures to TRAIL-induced apoptosis, which also occurred through the caspase-8-initiated caspase cascade. Etoposide 105-114 caspase 8 Homo sapiens 232-241 12764618-4 2003 Using cleavage site-directed antibodies, specific intracellular detection for cleaved fragments of caspase-8 and -9 was accomplished during apoptosis induced by staurosporine and etoposide. Etoposide 179-188 caspase 8 Homo sapiens 99-115 10318846-0 1999 Common regulation of apoptosis signaling induced by CD95 and the DNA-damaging stimuli etoposide and gamma-radiation downstream from caspase-8 activation. Etoposide 86-95 caspase 8 Homo sapiens 132-141 11861801-4 2002 Pretreatment with a broad caspase inhibitor [benzyloxycarbonyl-Val-Ala-Asp-(Ome) fluoromethyl ketone] markedly decreased the incidence of apoptotic cells induced by FTY720, etoposide, and anti-Fas antibody, through the abrogation of cleavage of Bid, poly(ADP-ribose) polymerase, and caspases 3, 8, and 9. Etoposide 173-182 caspase 8 Homo sapiens 26-33 11604558-7 2001 Hence, this study provides support for caspase-8-mediated apoptosis in U-937 GTB when exposed to etoposide. Etoposide 97-106 caspase 8 Homo sapiens 39-48 10749135-7 2000 In contrast, a transient transfection of dominant negative caspase-8 or CrmA or exposure to caspase-8 inhibitor zIETD-fmk inhibited the processing of procaspase-8 and Bid but did not inhibit the cytosolic accumulation of cyt c in either the untreated HL-60/Apaf-1 cells or the etoposide-treated HL-60/Apaf-1 and HL-60/neo cells. Etoposide 277-286 caspase 8 Homo sapiens 59-68 10749135-7 2000 In contrast, a transient transfection of dominant negative caspase-8 or CrmA or exposure to caspase-8 inhibitor zIETD-fmk inhibited the processing of procaspase-8 and Bid but did not inhibit the cytosolic accumulation of cyt c in either the untreated HL-60/Apaf-1 cells or the etoposide-treated HL-60/Apaf-1 and HL-60/neo cells. Etoposide 277-286 caspase 8 Homo sapiens 92-101 10216102-3 1999 Because apoptosis induced by anticancer drugs has been proposed to involve CD95/CD95 ligand interaction, we investigated the mechanism of caspase activation by daunorubicin, doxorubicin, etoposide, and mitomycin C. Etoposide 187-196 caspase 8 Homo sapiens 138-145 10022243-1 1998 Apoptosis, induced in human monocytic THP.1 cells by etoposide and N-tosyl-L-phenylalanyl chloromethyl ketone, was accompanied by the processing/activation of caspases, externalisation of phosphatidylserine (PS) and reduction in mitochondrial membrane potential (delta psi(m)). Etoposide 53-62 caspase 8 Homo sapiens 159-167 10194469-6 1999 These results indicate that the caspases required for the Cer response to etoposide and IR reside at or downstream from the mitochondria. Etoposide 74-83 caspase 8 Homo sapiens 32-40 26622554-6 2015 Furthermore, the caspase-3, caspase-8 and caspase-9 activities in etoposide-induced apoptosis demonstrated a greater increase upon neuraminidase pretreatment compared with no neuraminidase pretreatment. Etoposide 66-75 caspase 8 Homo sapiens 28-37 34363313-4 2021 We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells. Etoposide 47-56 caspase 8 Homo sapiens 194-203 34363313-4 2021 We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells. Etoposide 47-56 caspase 8 Homo sapiens 240-248 33194045-12 2020 Additionally, knockdown of caspase-8 reduced the doxorubicin, carboplatin, cisplatin, and etoposide sensitivity towards A549 cells. Etoposide 90-99 caspase 8 Homo sapiens 27-36 14646514-0 1998 The anti-cancer drug etoposide can induce caspase-8 processing and apoptosis in the absence of CD95 receptor-ligand interaction. Etoposide 21-30 caspase 8 Homo sapiens 42-51 14646514-2 1998 We find that, in Jurkat T cells, the DNA damaging anti-cancer drug etoposide induces apoptosis and, surprisingly, processing of caspase-8. Etoposide 67-76 caspase 8 Homo sapiens 128-137 14646514-6 1998 Apparently, in Jurkat cells, etoposide can induce caspase-8 processing and apoptosis in a CD95-independent fashion. Etoposide 29-38 caspase 8 Homo sapiens 50-59 27993669-6 2017 Suppression of etoposide-induced cell death correlated with a downregulation of p53 expression, which, among other functions, regulates the expression of death receptor 5, one of the activators of caspase-8. Etoposide 15-24 caspase 8 Homo sapiens 197-206 24436715-11 2013 In the human NP cells, NCCM inhibits Etoposide- mediated apoptosis via suppression of activated caspase-8, caspase-9, and mainly caspase-3/7. Etoposide 37-46 caspase 8 Homo sapiens 96-105 23124518-0 2012 Etoposide sensitizes neuroblastoma cells expressing caspase 8 to TRAIL. Etoposide 0-9 caspase 8 Homo sapiens 52-61 23430060-9 2013 GP7- or etoposide-induced apoptotic DNA fragmentation of human OS cells was inhibited by the pan caspase inhibitor and caspase-9 inhibitor, not by caspase-8 inhibitor whereas it was not inhibited by the pan caspase inhibitor in mouse OS cells. Etoposide 8-17 caspase 8 Homo sapiens 147-156 23124518-6 2012 Moreover, pretreatment with etoposide increased TRAIL-induced apoptosis in caspase 8 restored IMR-32 cells through activation of a caspase cascade that included caspases 8, 9 and 3. Etoposide 28-37 caspase 8 Homo sapiens 75-84 23124518-6 2012 Moreover, pretreatment with etoposide increased TRAIL-induced apoptosis in caspase 8 restored IMR-32 cells through activation of a caspase cascade that included caspases 8, 9 and 3. Etoposide 28-37 caspase 8 Homo sapiens 161-180 23124518-7 2012 These results indicate that the etoposide-mediated sensitization of neuroblastoma cells to TRAIL is associated with an increase in TRAIL-R2 expression and requires caspase 8 expression. Etoposide 32-41 caspase 8 Homo sapiens 164-173 23124518-2 2012 We provide evidence that pretreatment with etoposide significantly enhanced TRAIL-mediated apoptosis via up-regulation of DR5 (death receptor 5 or TRAIL-R2) expression in the caspase 8 expressing neuroblastoma cell line, SK-N-MC. Etoposide 43-52 caspase 8 Homo sapiens 175-184 21801448-0 2011 Essential role of caspase-8 in p53/p73-dependent apoptosis induced by etoposide in head and neck carcinoma cells. Etoposide 70-79 caspase 8 Homo sapiens 18-27 21801448-11 2011 Our data suggest the importance of caspase-8-mediated positive feedback amplification in the p53/p73-dependent apoptosis induced by etoposide in HNSCC cells. Etoposide 132-141 caspase 8 Homo sapiens 35-44 21801448-4 2011 RESULTS: We show that p53/p73-dependent caspase-8 activation is required for sensitizing etoposide-induced apoptosis by utilizing HOC313 cells carrying a temperature-sensitive p53G285K mutant. Etoposide 89-98 caspase 8 Homo sapiens 40-49 21801448-6 2011 In addition to p53 restoration, caspase-8 reconstitution was needed for sensitization to etoposide-induced apoptosis, mitochondria depolarization, and cleavage of the procaspases-3, and -9. Etoposide 89-98 caspase 8 Homo sapiens 32-41 21801448-9 2011 Finally, the caspase-9 inhibitor Ac-LEHD-CHO or caspase-9 siRNA blocked etoposide-induced caspase-8 activation, Bid cleavage, and apoptosis in both cell lines, indicating that p53/p73-dependent caspase-8 activation lies downstream of mitochondria. Etoposide 72-81 caspase 8 Homo sapiens 90-99 21801448-9 2011 Finally, the caspase-9 inhibitor Ac-LEHD-CHO or caspase-9 siRNA blocked etoposide-induced caspase-8 activation, Bid cleavage, and apoptosis in both cell lines, indicating that p53/p73-dependent caspase-8 activation lies downstream of mitochondria. Etoposide 72-81 caspase 8 Homo sapiens 194-203 21801448-10 2011 CONCLUSIONS: we conclude that p53 and p73 can act as upstream regulators of caspase-8, and that caspase-8 is an essential mediator of the p53/p73-dependent apoptosis induced by etoposide in HNSCC cells. Etoposide 177-186 caspase 8 Homo sapiens 96-105 21468663-4 2011 In this study, we showed that etoposide treatment activated caspase-8 and caspase-3, leading to cleavages of p53, Bid and PARP, which subsequently induced apoptosis. Etoposide 30-39 caspase 8 Homo sapiens 60-69 20416058-4 2010 RESULTS: We demonstrated that doxorubicin and etoposide markedly sensitized SCLC cells expressing caspase-8 to apoptotic effects of TRAIL. Etoposide 46-55 caspase 8 Homo sapiens 98-107 20416058-0 2010 Doxorubicin and etoposide sensitize small cell lung carcinoma cells expressing caspase-8 to TRAIL. Etoposide 16-25 caspase 8 Homo sapiens 79-88 20416058-8 2010 CONCLUSIONS: Our results highlight significant applicability of doxorubicin and etoposide in sensitization of SCLC cells expressing caspase-8 to treatment with TRAIL. Etoposide 80-89 caspase 8 Homo sapiens 132-141 17694514-8 2007 Inhibition of caspase-9 specifically reduced v-Myc-stimulated apoptosis, whereas inhibition of caspase-8 and -3/7 reduced apoptosis both in v-myc-expressing and parental ETO-treated U-937 cells. Etoposide 170-173 caspase 8 Homo sapiens 95-111 19549763-3 2009 Treatment of cells with the caspase-3-specific inhibitor N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethyl ketone or caspase-3-specific small interacting RNA (siRNA) prevented the etoposide-induced activation of caspase-8 and inhibited apoptosis. Etoposide 179-188 caspase 8 Homo sapiens 211-220 19549763-5 2009 Furthermore, the etoposide-induced processing of caspase-2 required the expression of caspase-8, and the etoposide-mediated processing of caspase-8 required the expression of caspase-2, indicating that these two caspases activate each other after etoposide treatment. Etoposide 17-26 caspase 8 Homo sapiens 86-95 19549763-5 2009 Furthermore, the etoposide-induced processing of caspase-2 required the expression of caspase-8, and the etoposide-mediated processing of caspase-8 required the expression of caspase-2, indicating that these two caspases activate each other after etoposide treatment. Etoposide 105-114 caspase 8 Homo sapiens 138-147 19549763-5 2009 Furthermore, the etoposide-induced processing of caspase-2 required the expression of caspase-8, and the etoposide-mediated processing of caspase-8 required the expression of caspase-2, indicating that these two caspases activate each other after etoposide treatment. Etoposide 105-114 caspase 8 Homo sapiens 138-147 19549763-6 2009 We also observed that etoposide-mediated apoptosis was decreased by treating the cells with the caspase-6-specific inhibitor benzyloxycarbonyl-Val-Glu(OMe)-Ile-Asp-(OMe)-fluoromethyl ketone and that caspase-6 was activated by a caspase-8-dependent mechanism. Etoposide 22-31 caspase 8 Homo sapiens 228-237 19549763-7 2009 Finally, we show that rottlerin blocks etoposide-induced apoptosis by inhibiting the PKCdelta-mediated activation of caspase-3 and by degrading caspase-2, which prevents caspase-8 activation. Etoposide 39-48 caspase 8 Homo sapiens 170-179 17627812-2 2007 In this study, IFN-gamma mediated up-regulation of caspase-8 in human MB cells was found to result in chemosensitization to cisplatin, doxorubicin and etoposide, and sensitisation to radiation. Etoposide 151-160 caspase 8 Homo sapiens 51-60