PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28553347-6 2017 Mitomycin C upregulated the expression levels of Fas, DR4, DR5, cleaved caspase-8/9, Bax, Bim and cleaved caspase-3 proteins, and it downregulated Bcl-2 and Bcl-xL expression. Mitomycin 0-11 caspase 8 Homo sapiens 72-83 29467593-8 2018 Caspase activation was assessed by MTT and PI after treatments with Z-VAD [OME]-FMK, mitomycin c and cycloheximide. Mitomycin 85-96 caspase 8 Homo sapiens 0-7 29467593-14 2018 Subsequent activation of caspase-8 after co-incubation of mitomycin c and cycloheximide separately, restored the cell viability in cholesterol depleted MDA-MB 231 cells. Mitomycin 58-69 caspase 8 Homo sapiens 25-34 21616659-8 2011 MMC and curcumin together synergistically enhanced apoptosis in MCF-7 cells and the apoptosis most likely resulted from both the activation of caspases and modulation of bcl-2/bax expression. Mitomycin 0-3 caspase 8 Homo sapiens 143-151 27462786-2 2016 In the present study we aimed to investigate the clinical relevance of Plk3 expression and phosphorylation of caspase-8 at T273 in patients with anal squamous cell carcinoma (SSC) treated with 5-fluorouracil and mitomycin C-based chemoradiotherapy (CRT). Mitomycin 212-223 caspase 8 Homo sapiens 110-119 18806879-10 2008 CONCLUSIONS: These results indicate that mitomycin-induced cellular apoptosis in corneal endothelial cells may be mediated through caspase-8, caspase-9, and the mitochondrial regulated pathways as well as through upregulation of p53-dependent and p21-dependent signal transduction pathways. Mitomycin 41-50 caspase 8 Homo sapiens 131-140 17021654-6 2007 Both mitomycin C and cisplatin induced apoptosis in C-33A cells via caspase-8 and -3 processing in a Fas/FasL-dependent manner and also suppressed IL-18 expression, while they down-regulated IkappaB expression and up-regulated p65 expression. Mitomycin 5-16 caspase 8 Homo sapiens 68-84 17922191-0 2007 Molecular mechanism of Mitomycin C-dependent caspase-8 regulation: implications for apoptosis and synergism with interferon-alpha signalling. Mitomycin 23-34 caspase 8 Homo sapiens 45-54 17922191-5 2007 However, strong caspase-8 promoter induction was found after Mitomycin C (MMC) treatment and this correlated with an increase in endogenous caspase-8 mRNA expression. Mitomycin 61-72 caspase 8 Homo sapiens 16-25 17922191-5 2007 However, strong caspase-8 promoter induction was found after Mitomycin C (MMC) treatment and this correlated with an increase in endogenous caspase-8 mRNA expression. Mitomycin 61-72 caspase 8 Homo sapiens 140-149 17922191-5 2007 However, strong caspase-8 promoter induction was found after Mitomycin C (MMC) treatment and this correlated with an increase in endogenous caspase-8 mRNA expression. Mitomycin 74-77 caspase 8 Homo sapiens 16-25 17922191-5 2007 However, strong caspase-8 promoter induction was found after Mitomycin C (MMC) treatment and this correlated with an increase in endogenous caspase-8 mRNA expression. Mitomycin 74-77 caspase 8 Homo sapiens 140-149 17922191-8 2007 MMC treatment resulted in higher caspase-8 enzymatic activity and apoptosis and could be synergistically enhanced by co-stimulation with interferon-alpha (IFNalpha) via independent transcriptional mechanisms. Mitomycin 0-3 caspase 8 Homo sapiens 33-42 17652735-12 2007 Caspase-8, caspase-3, and broad caspase inhibitors, but not caspase-9 inhibitor, inhibited MMC-induced cell death in nonpretreated and IFN-pretreated cells. Mitomycin 91-94 caspase 8 Homo sapiens 0-9 17652735-12 2007 Caspase-8, caspase-3, and broad caspase inhibitors, but not caspase-9 inhibitor, inhibited MMC-induced cell death in nonpretreated and IFN-pretreated cells. Mitomycin 91-94 caspase 8 Homo sapiens 11-18 17021654-7 2007 These results suggest that both mitomycin C and cisplatin induce apoptosis, not only via the caspase-8 and -3 dependent Fas/FasL pathway, but also via the regulation of NF-kappaB activity and IL-18 expression in HPV-negative cervical cancer C-33A cells. Mitomycin 32-43 caspase 8 Homo sapiens 93-109 15450951-3 2004 The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO). Mitomycin 4-7 caspase 8 Homo sapiens 92-99 16186332-10 2005 CONCLUSIONS: Mitomycin-C induced the apoptosis of HTCFs through the activation of intrinsic and extrinsic caspase cascades with mitochondrial dysfunction. Mitomycin 13-24 caspase 8 Homo sapiens 106-113 16019139-8 2006 Our results indicated that MMC induced apoptosis in SiHa/pRSV-luc and SiHa cells via caspase-8 and -3 processing, in a Fas/FasL-dependent manner. Mitomycin 27-30 caspase 8 Homo sapiens 85-101 16019139-11 2006 These results suggest that MMC induces apoptosis, not only through caspase-8 and -3 dependent Fas/FasL pathway, but also via the regulation of NF-kappaB activity and IL-18 expression. Mitomycin 27-30 caspase 8 Homo sapiens 67-83 12181741-0 2002 Mitomycin C induces apoptosis and caspase-8 and -9 processing through a caspase-3 and Fas-independent pathway. Mitomycin 0-11 caspase 8 Homo sapiens 34-50 12181741-5 2002 MMC treatment led to pronounced caspase-8, -9, and -7 processing and early morphological features of apoptosis within 48 h. This could be inhibited by the broad-spectrum caspase inhibitor z-VAD.fmk and to a lesser extent by z-IETD.fmk and z-LEHD.fmk, which have a certain preference for inhibiting caspase-8 and -9, respectively. Mitomycin 0-3 caspase 8 Homo sapiens 32-41 12181741-5 2002 MMC treatment led to pronounced caspase-8, -9, and -7 processing and early morphological features of apoptosis within 48 h. This could be inhibited by the broad-spectrum caspase inhibitor z-VAD.fmk and to a lesser extent by z-IETD.fmk and z-LEHD.fmk, which have a certain preference for inhibiting caspase-8 and -9, respectively. Mitomycin 0-3 caspase 8 Homo sapiens 298-314 12181741-6 2002 MMC induced apoptosis in MCF-7 cells was not mediated by the death receptor pathway as demonstrated by experiments using the inhibiting anti-Fas antibody ZB4 and transfections with CrmA, a viral serpin inhibitor of caspase-8, and the dominant negative Fas-associated death domain (FADD-DN). Mitomycin 0-3 caspase 8 Homo sapiens 215-224 11525634-9 2001 Caspase-8 activation by MMC evokes the mitochondrial pathways involving FANCC but not ATM. Mitomycin 24-27 caspase 8 Homo sapiens 0-9 10960761-2 2000 Caspase-8 and caspase-3 were activated in MMC-treated cells whereas caspase-1 was not activated, and cytochrome c was released from mitochondrial membrane to cytosol suggesting that caspase-9 was activated during the MMC-induced apoptotic process. Mitomycin 42-45 caspase 8 Homo sapiens 0-9 10960761-5 2000 Activation of caspase-8 in response to Fas triggering by recruitment of caspase-8 to the Fas has also been found, however, MMC did not induce FasL and Fas expression, as evidenced by reverse transcriptase-polymerase chain reaction and Western blotting. Mitomycin 123-126 caspase 8 Homo sapiens 14-23 10960761-6 2000 Taken together, these findings indicate that MMC-induced apoptosis in SNU-16 cells was mediated by caspase-8, caspase-9, and caspase-3 activation independently of FasL/Fas interactions. Mitomycin 45-48 caspase 8 Homo sapiens 99-108 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. Mitomycin 202-213 caspase 8 Homo sapiens 138-145