PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17119454-6 2006 We analysed dose-dependent release of cytochrome c, caspase-9 activation, cleavage of PARP and activation of effector caspases in etoposide and cisplatin-resistant cells after exposure to etoposide, teniposide, cisplatin or fotemustine. Etoposide 130-139 caspase 9 Homo sapiens 118-126 20888374-8 2011 Different from the cases with FR or sulforaphane, etoposide- or doxorubicin-induced cell death was suppressed with co-treatment of caspase-9 inhibitor, and the drugs failed to induce significant autophagy in MCF-7 cells. Etoposide 50-59 caspase 9 Homo sapiens 131-140 17119454-6 2006 We analysed dose-dependent release of cytochrome c, caspase-9 activation, cleavage of PARP and activation of effector caspases in etoposide and cisplatin-resistant cells after exposure to etoposide, teniposide, cisplatin or fotemustine. Etoposide 188-197 caspase 9 Homo sapiens 118-126 15388581-4 2005 Ectopic expression of hsp70 in HL-60 cells (HL-60/hsp70) inhibited Ara-C and etoposide-induced Bax conformation change and translocation to the mitochondria; attenuated the accumulation of cytochrome c, Smac, and Omi/HtrA2 in the cytosol; and inhibited the processing and activity of caspase-9 and caspase-3. Etoposide 77-86 caspase 9 Homo sapiens 284-293 16575541-5 2006 Caspase activity assay showed that our peptide successfully increased the activity of caspase-3 and caspase-9 in etoposide-induced apoptosis. Etoposide 113-122 caspase 9 Homo sapiens 100-109 15876872-3 2005 Furthermore, functional analysis of apoptosis sensitivity showed that lymphomas with a caspase 9 inhibition profile were indeed relatively resistant to Etoposide induced apoptosis. Etoposide 152-161 caspase 9 Homo sapiens 87-96 16895478-0 2006 Treatment of MCF-7 cells with taxol and etoposide induces distinct alterations in the expression of apoptosis-related genes BCL2, BCL2L12, BAX, CASPASE-9 and FAS. Etoposide 40-49 caspase 9 Homo sapiens 144-153 16895478-3 2006 In the case of etoposide, down-regulation of the BCL2L12-A gene variant and of CASPASE-9, as well as upregulation of BAX, was observed, whereas treatment of MCF-7 cells with taxol led to down-regulation of the mRNA levels of all genes examined. Etoposide 15-24 caspase 9 Homo sapiens 79-88 16204039-6 2005 Its overexpression inhibited pro-caspase-9 activation, leading to the suppression of the cell death induced by a protein kinase inhibitor, staurosporine, or a chemotherapeutic reagent, etoposide (VP-16). Etoposide 185-194 caspase 9 Homo sapiens 33-42 16204039-6 2005 Its overexpression inhibited pro-caspase-9 activation, leading to the suppression of the cell death induced by a protein kinase inhibitor, staurosporine, or a chemotherapeutic reagent, etoposide (VP-16). Etoposide 196-201 caspase 9 Homo sapiens 33-42 15817479-4 2005 Stress stimuli, including ceramide and etoposide, caused caspase-2 activation, mitochondrial damage followed by downstream caspase-9 and -3 activation, and cell apoptosis in human lung epithelial cell line A549. Etoposide 39-48 caspase 9 Homo sapiens 123-139 15492260-5 2004 Treatment with cisplatin, camptothecin, etoposide, betulinic acid, celecoxib, 1400W, and staurosporine promoted enzymatic activity not only of caspases -2, -8, and -3 but also of caspase-9 in both APAF-1(+) and APAF-1(-) tumor cells. Etoposide 40-49 caspase 9 Homo sapiens 179-188 14745596-14 2004 Etoposide induced cleavage of caspase-9 in both cell lines, with the EBV-positive cells having proportionally less cleavage product, in agreement with their lower levels of apoptosis. Etoposide 0-9 caspase 9 Homo sapiens 30-39 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 9 Homo sapiens 119-128 14672900-7 2004 LLL-CHO, etoposide, and C2-ceramide also caused DeltaPsim, the increment of both hypodiploid DNA(+) cells and TUNEL(+) cells, and the activation of both Leu-Glu-His-Asp ase (LEHDase; caspase-9 like activity) and Asp-Glu-Val-Asp ase (DEVDase; caspase-3 like activity) in synovial cells. Etoposide 9-18 caspase 9 Homo sapiens 183-192 12121973-8 2002 Treatment of NCI-H82 cells with etoposide induces a series of time-dependent events, including the release of cytochrome c from the mitochondria to the cytosol, activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase (PARP). Etoposide 32-41 caspase 9 Homo sapiens 175-184 11912135-6 2002 In contrast, SNAP did prevent activation of caspase 9 in etoposide-treated cells. Etoposide 57-66 caspase 9 Homo sapiens 44-53 11791171-5 2002 In PA1-neo cells with wild-type p53, the activation of caspases including caspases 9, 8, 7 and 3 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such changes were observed in PA1-E6 cells whose p53 is degraded, suggesting that loss of p53 impairs caspase activation. Etoposide 156-165 caspase 9 Homo sapiens 55-62 11901191-9 2002 Furthermore, the specific caspase-9 inhibitor LEHD-fmk significantly inhibited etoposide-induced nSMase activation, Cer accumulation, and PKCdelta mitochondrial translocation. Etoposide 79-88 caspase 9 Homo sapiens 26-35 11346470-4 2001 The degree of apoptosis in etoposide-treated U-373MG cells infected with Adv for Apaf-1 (Adv-APAF1) was higher (27%) than that in cells infected with control Adv (14%), that in cells infected with Adv for caspase-9 (Adv-Casp9) was higher (34%) than that in cells infected with Adv-APAF1, and that in cells infected with both Adv-APAF1 and Adv-Casp9 was the highest (41%). Etoposide 27-36 caspase 9 Homo sapiens 205-214 11346470-0 2001 Co-transduction of Apaf-1 and caspase-9 augments etoposide-induced apoptosis in U-373MG glioma cells. Etoposide 49-58 caspase 9 Homo sapiens 30-39 11346470-4 2001 The degree of apoptosis in etoposide-treated U-373MG cells infected with Adv for Apaf-1 (Adv-APAF1) was higher (27%) than that in cells infected with control Adv (14%), that in cells infected with Adv for caspase-9 (Adv-Casp9) was higher (34%) than that in cells infected with Adv-APAF1, and that in cells infected with both Adv-APAF1 and Adv-Casp9 was the highest (41%). Etoposide 27-36 caspase 9 Homo sapiens 216-225 11346470-4 2001 The degree of apoptosis in etoposide-treated U-373MG cells infected with Adv for Apaf-1 (Adv-APAF1) was higher (27%) than that in cells infected with control Adv (14%), that in cells infected with Adv for caspase-9 (Adv-Casp9) was higher (34%) than that in cells infected with Adv-APAF1, and that in cells infected with both Adv-APAF1 and Adv-Casp9 was the highest (41%). Etoposide 27-36 caspase 9 Homo sapiens 339-348 11033421-6 2000 (2) Delayed addition of H(2)O(2) to VP-16-treated cells prevents additional caspase induction but does not inhibit the caspase activity that has already been generated. Etoposide 36-41 caspase 9 Homo sapiens 76-83 11042671-3 2000 Etoposide induced increased formation of ceramide from sphingomyelin and release of mitochondrial cytochrome c followed by activation of caspase-9 and caspase-3, but not caspase-1. Etoposide 0-9 caspase 9 Homo sapiens 137-146 11042671-9 2000 Taken together, these results suggest that ceramide may function as a mediator of etoposide-induced apoptosis of C6 glioma cells, which induces increase in the Bax/Bcl-2 ratio followed by release of cytochrome c leading to caspases-9 and -3 activation. Etoposide 82-91 caspase 9 Homo sapiens 223-240 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 9 Homo sapiens 252-261 34674796-9 2022 These results combined indicate that PEMFs enhance etoposide-induced cell death by increasing ROS induction-DNA damage-caspase-dependent apoptosis. Etoposide 51-60 caspase 9 Homo sapiens 119-126 10544189-9 1999 We conclude that HSP27 inhibits etoposide-induced apoptosis by preventing cytochrome c and dATP-triggered activity of caspase-9, downstream of cytochrome c release. Etoposide 32-41 caspase 9 Homo sapiens 118-127 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. Etoposide 120-129 caspase 9 Homo sapiens 270-279 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 9 Homo sapiens 107-116 26424010-4 2015 SPATA4 protected HeLa cells from etoposide-induced apoptosis through the mitochondrial apoptotic pathway, in the way that SPATA4 suppressed decrease of the mitochondrial membrane potential, the release of cytochrome c, and subsequent activation of caspase-9 and -3. Etoposide 33-42 caspase 9 Homo sapiens 248-264 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 9 Homo sapiens 42-51 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 9 Homo sapiens 13-22 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 9 Homo sapiens 119-128 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 9 Homo sapiens 48-57