PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33985619-3 2022 c-Src-mediated Caspase-8 phosphorylation essential for EMT in lung adenocarcinoma cell lines preferentially occurs in cells with the mesenchymal phenotype, resulting in chemoresistance to cisplatin plus paclitaxel inpatients with resectable lung adenocarcinoma and a significantly worse 5-year PFS. Cisplatin 188-197 caspase 8 Homo sapiens 15-24 31838086-6 2020 Efficacy of the combined treatment relied on cisplatin-induced downregulation of c-FLIP, the main regulator of the extrinsic apoptotic pathway, leading to an enhanced caspase-8-mediated pathway. Cisplatin 45-54 caspase 8 Homo sapiens 167-176 33194045-12 2020 Additionally, knockdown of caspase-8 reduced the doxorubicin, carboplatin, cisplatin, and etoposide sensitivity towards A549 cells. Cisplatin 75-84 caspase 8 Homo sapiens 27-36 31571909-9 2019 Chitin oligosaccharide plus cisplatin up-regulated the expression level of caspase8 and caspase3, while had minor influence on the expression level of BAK. Cisplatin 28-37 caspase 8 Homo sapiens 75-83 32187278-8 2020 CASPASE-8 and TNFRSF10B expression levels could predict the response of both the cell lines to rhTRAIL alone or the response to a combination of rhTRAIL and cisplatin. Cisplatin 157-166 caspase 8 Homo sapiens 0-9 31587185-1 2019 The objective of this research was to assess the association of genetic polymorphisms related to intrinsic apoptosis pathway CASP8 rs3834129 and CASP3 rs4647601 with the risk, clinical and pathological aspects, and survival of oropharynx squamous cell carcinoma (OPSCC) patients that received cisplatin and radiotherapy. Cisplatin 293-302 caspase 8 Homo sapiens 125-130 31571909-11 2019 Conclusion: The study demonstrated that chitin oligosaccharide plus cisplatin had positive synergistic effects, and it is possible to improve the prognosis of lung adenocarcinoma patients by up-regulating the expression level of caspase8, caspase3 and down-regulating the expression level of Ki67. Cisplatin 68-77 caspase 8 Homo sapiens 229-237 30724400-10 2019 CONCLUSIONS: N-myc and caspase-8 expressions are involved in TRAIL susceptibility in IMR-32 cells, and the combination of treatment with cisplatin and TRAIL may serve as a promising strategy for the development of therapeutics against neuroblastoma that is controlled by N-myc and caspase-8 expression. Cisplatin 137-146 caspase 8 Homo sapiens 23-32 30941888-7 2019 Collectively, our study demonstrates that p62 promotes Caspase 8 activation through autophagy flux blockage with cisplatin treatment. Cisplatin 113-122 caspase 8 Homo sapiens 55-64 30724400-10 2019 CONCLUSIONS: N-myc and caspase-8 expressions are involved in TRAIL susceptibility in IMR-32 cells, and the combination of treatment with cisplatin and TRAIL may serve as a promising strategy for the development of therapeutics against neuroblastoma that is controlled by N-myc and caspase-8 expression. Cisplatin 137-146 caspase 8 Homo sapiens 281-290 30944654-8 2019 Subsequent mechanistic analysis demonstrated that TNFAIP8 silencing promoted caspase-8/-3 activation and p38 phosphorylation in HeLa cells treated with cisplatin, whereas apoptosis regulator B-cell lymphoma-2 expression was inhibited with TNFAIP8-silenced HeLa cells following treatment with cisplatin. Cisplatin 152-161 caspase 8 Homo sapiens 77-86 30868675-9 2019 Further study showed that CAF-CM enhanced cisplatin resistance by inhibiting cisplatin-induced apoptosis, determined by repression of caspase-3 and caspase-8, through activation of the ANXA3/JNK pathway. Cisplatin 77-86 caspase 8 Homo sapiens 148-157 30867764-9 2019 In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged. Cisplatin 44-53 caspase 8 Homo sapiens 310-319 27871859-9 2017 Interestingly, in HO8910PM cells with ST3Gal3 knockdown, the levels of caspase 8 and caspase 3 proteins increased, which was more obvious in cells treated with both ST3Gal3 knockdown and cisplatin, suggesting that ST3Gal3 knockdown synergistically enhanced cisplatin-induced apoptosis in ovarian cancer cells. Cisplatin 187-196 caspase 8 Homo sapiens 71-80 27993669-7 2017 In contrast, stimulation of cisplatin-induced cell death involved reactive oxygen species-mediated downregulation of FLIP-S, an inhibitor of caspase-8. Cisplatin 28-37 caspase 8 Homo sapiens 141-150 30805008-6 2019 Interestingly, cisplatin upregulated critical components of the extrinsic apoptotic pathway-initiator caspase 8, effector caspase 3, and the cell death receptors. Cisplatin 15-24 caspase 8 Homo sapiens 102-111 30805008-8 2019 Finally, we have demonstrated the central role of caspase 8 in this process, since its downregulation abrogated the sensitizing effect of cisplatin. Cisplatin 138-147 caspase 8 Homo sapiens 50-59 28107698-11 2017 The combination of the IC50 doses of apigenin (15muM) and cisplatin (7.5muM) for 48h significantly enhanced cisplatin"s cytotoxic and apoptotic effects through downregulation of Bcl-2, sharpin and survivin; and upregulation of caspase-8, Apaf-1 and p53 mRNA expression. Cisplatin 58-67 caspase 8 Homo sapiens 227-236 27871859-9 2017 Interestingly, in HO8910PM cells with ST3Gal3 knockdown, the levels of caspase 8 and caspase 3 proteins increased, which was more obvious in cells treated with both ST3Gal3 knockdown and cisplatin, suggesting that ST3Gal3 knockdown synergistically enhanced cisplatin-induced apoptosis in ovarian cancer cells. Cisplatin 257-266 caspase 8 Homo sapiens 71-80 27473145-5 2016 However, combined treatment with GA and CDDP revealed a strong synergistic action between these drugs, and higher protein levels of the apoptosis-related factor Fas, cleaved caspase-8 and cleaved caspase-3 and lower expression of hypoxia-inducible factor (HIF)-1alpha are detected in both cell lines. Cisplatin 40-44 caspase 8 Homo sapiens 174-183 26796280-2 2016 Cisplatin may initiate p73-dependent apoptosis in p53 mutant cell lines through Fas trimerization and Caspase-8 activation and Bax up regulation and subsequent Caspase-9 activation. Cisplatin 0-9 caspase 8 Homo sapiens 102-111 27195913-4 2016 The present study reported that phosphorylated caspase-8 at tyrosine 380 (p-Casp8) was characterized as a biomarker of chemoresistance to TP regimen (cisplatin and paclitaxel) in patients with resectable lung adenocarcinoma with significantly poorer 5-year disease-free survival (DFS) and overall survival (OS). Cisplatin 150-159 caspase 8 Homo sapiens 47-72 27195913-4 2016 The present study reported that phosphorylated caspase-8 at tyrosine 380 (p-Casp8) was characterized as a biomarker of chemoresistance to TP regimen (cisplatin and paclitaxel) in patients with resectable lung adenocarcinoma with significantly poorer 5-year disease-free survival (DFS) and overall survival (OS). Cisplatin 150-159 caspase 8 Homo sapiens 76-81 27494891-6 2016 Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP. Cisplatin 79-88 caspase 8 Homo sapiens 303-312 26796280-7 2016 Higher Caspase-8 activity in the Lifeguard knockdown MDA after cisplatin administration could explain the significant decrease in cell viability from 24 to 48h. Cisplatin 63-72 caspase 8 Homo sapiens 7-16 26273359-8 2015 Furthermore, the treatment of A549 cells with TSA and cisplatin resulted in a significant decrease of pro-caspase-8 and a significant increase of caspase-8. Cisplatin 54-63 caspase 8 Homo sapiens 106-115 26171069-7 2015 Furthermore, enhanced protein expression of caspase-8 and -9, in line with the significantly increased caspase-3 activation, was detected when the cells were treated with a combination of cisplatin and bortezomib, compared with that of either agent alone. Cisplatin 188-197 caspase 8 Homo sapiens 44-60 25894537-6 2015 Increased caspase-8 and -9 activation was induced by cisplatin in C2 as compared to NT3 cells. Cisplatin 53-62 caspase 8 Homo sapiens 10-26 25770930-5 2015 In addition, combination of chrysin and cisplatin promoted both extrinsic apoptosis by activating caspase-8 and intrinsic apoptosis by increasing the release of cytochrome c and activating caspase-9 in Hep G2 cells. Cisplatin 40-49 caspase 8 Homo sapiens 98-107 26273359-8 2015 Furthermore, the treatment of A549 cells with TSA and cisplatin resulted in a significant decrease of pro-caspase-8 and a significant increase of caspase-8. Cisplatin 54-63 caspase 8 Homo sapiens 146-155 25085582-9 2014 The enhanced antitumor effects in vitro elicited by Ad/PSCAE/UPII/E1A plus cisplatin were closely related to the increased Fas expression and cleavage of caspase-8 and Bid and decrease in the ratio of anti- to pro-apoptotic proteins followed by activation of caspase-9 and caspase-3, which may contribute to the activation of extrinsic and intrinsic apoptotic pathways. Cisplatin 75-84 caspase 8 Homo sapiens 154-163 25682199-7 2015 Furthermore, the cisplatin and Chal-24 combination induced dramatic degradation of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein large (cFLIPL) which suppresses Ripoptosome-mediated apoptosis activation. Cisplatin 17-26 caspase 8 Homo sapiens 92-97 25682199-7 2015 Furthermore, the cisplatin and Chal-24 combination induced dramatic degradation of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein large (cFLIPL) which suppresses Ripoptosome-mediated apoptosis activation. Cisplatin 17-26 caspase 8 Homo sapiens 99-135 24894297-0 2014 Targeting Notch1 signaling pathway positively affects the sensitivity of osteosarcoma to cisplatin by regulating the expression and/or activity of Caspase family. Cisplatin 89-98 caspase 8 Homo sapiens 147-154 25216531-5 2014 Apollon knockdown also enhanced cisplatin/docetaxel-induced activation of caspase-8 (extrinsic pathway) and caspase-9 (intrinsic pathway) in ESCC cells and xenograft tumor models. Cisplatin 32-41 caspase 8 Homo sapiens 74-83 24519546-8 2014 Cisplatin sensitivity analysis and cisplatin-induced activation of caspase 8 analysis were also performed. Cisplatin 35-44 caspase 8 Homo sapiens 67-76 24894297-10 2014 Further mechanism investigation revealed that activation/inhibition of Notch1 sensitized/desensitized cisplatin-induced apoptosis, which probably depended on the changes in the activity of Caspase family, including Caspase 3, Caspase 8 and Caspase 9 in these cells. Cisplatin 102-111 caspase 8 Homo sapiens 189-196 24894297-10 2014 Further mechanism investigation revealed that activation/inhibition of Notch1 sensitized/desensitized cisplatin-induced apoptosis, which probably depended on the changes in the activity of Caspase family, including Caspase 3, Caspase 8 and Caspase 9 in these cells. Cisplatin 102-111 caspase 8 Homo sapiens 226-235 23912708-9 2013 Moreover, the induction of apoptosis by TRAIL plus cisplatin was accompanied by the downregulation of cFLIP and BCL2L1, and simultaneously robust enzymatic activation of caspase-8, culminating in decreased cancer cell survival. Cisplatin 51-60 caspase 8 Homo sapiens 170-179 24507386-14 2014 The tumor tissues were harvested after treatment, and ACBP-L and Cisplatin treatment suppressed Bcl-2, and induced Bax, Caspase 3, and Caspase 8 molecules as detected by RT-PCR and immunohistochemistry. Cisplatin 65-74 caspase 8 Homo sapiens 135-144 24286513-7 2014 The acetyl-L-carnitine-cisplatin combination caused reduced expression of genes Casp8, Fas, Casp1, Tnfrsf11b, Tnfrsf10b induced by cisplatin. Cisplatin 23-32 caspase 8 Homo sapiens 80-85 24286513-7 2014 The acetyl-L-carnitine-cisplatin combination caused reduced expression of genes Casp8, Fas, Casp1, Tnfrsf11b, Tnfrsf10b induced by cisplatin. Cisplatin 131-140 caspase 8 Homo sapiens 80-85 24286513-6 2014 Genes displaying increase in expression of apoptosis, related to cisplatin treatment, were Casp8, Bcl10, Bcl2, Bcl2l1, Bcl2l2, Bid, Naip1, Bnip3l, Card6, Pak7, Cd40, Trp 53inp1, Cideb and Cd70. Cisplatin 65-74 caspase 8 Homo sapiens 91-96 24309938-7 2013 In addition, HDAC inhibitors synergized with TRAIL and cisplatin in NSCLC cells in a FLIP- and caspase-8-dependent manner. Cisplatin 55-64 caspase 8 Homo sapiens 95-104 23830991-10 2013 The results suggested that combination of crocin and cisplatin has a strong killing effect on osteosarcoma cells and suppresses the ability of invasion of MG63 and OS732 cells which might be related to up-regulate the expression of caspase-3 and caspase-8. Cisplatin 53-62 caspase 8 Homo sapiens 246-255 22328720-8 2012 Cisplatin in combination with death receptor ligands enhanced caspase-8 and caspase-3 activation and reduced X-linked inhibitor-of-apoptosis protein (XIAP) levels in these cells. Cisplatin 0-9 caspase 8 Homo sapiens 62-71 23826494-0 2013 Synergistic Effect of Subtoxic-dose Cisplatin and TRAIL to Mediate Apoptosis by Down-regulating Decoy Receptor 2 and Up-regulating Caspase-8, Caspase-9 and Bax Expression on NCI-H460 and A549 Cells. Cisplatin 36-45 caspase 8 Homo sapiens 131-140 23564782-7 2013 Collectively, these results suggest that beta-elemene augments the antitumor activity of cisplatin in human bladder cancer by enhancing the induction of cellular apoptosis via a caspase-dependent mechanism. Cisplatin 89-98 caspase 8 Homo sapiens 178-185 23564786-12 2013 CONCLUSION: These findings provide important insights regarding the activation of caspase-8 and DR5, to our knowledge, for the first time in salinomycin-treated cisplatin-resistant ovarian cancer and demonstrate that salinomycin could be a prominent anticancer agent. Cisplatin 161-170 caspase 8 Homo sapiens 82-91 23254292-0 2012 Acquired differential regulation of caspase-8 in cisplatin-resistant non-small-cell lung cancer. Cisplatin 49-58 caspase 8 Homo sapiens 36-45 23254292-5 2012 In H460 NSCLC cells, caspase-8 cleavage was shown to be induced by cisplatin and is dependent on death receptor 4, death receptor 5, Fas-associated protein with death domain, acid sphingomyelinase and ceramide synthesis. Cisplatin 67-76 caspase 8 Homo sapiens 21-30 23254292-7 2012 Accordingly, caspase-8 activation block acquired during cisplatin resistance, can be bypassed by death receptor agonism. Cisplatin 56-65 caspase 8 Homo sapiens 13-22 23926438-6 2013 Furthermore, cordycepin or cisplatin induced caspase-8, caspase-9, caspase-3, and poly adenosine diphosphate-ribose polymerase protein cleavages, and stimulated c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, and p38 protein phosphorylations. Cisplatin 27-36 caspase 8 Homo sapiens 45-54 22431999-9 2012 In vitro studies demonstrated that MVs up-regulated in cisplatin-treated human tubular epithelial cells anti-apoptotic genes, such as Bcl-xL, Bcl2 and BIRC8 and down-regulated genes that have a central role in the execution-phase of cell apoptosis such as Casp1, Casp8 and LTA. Cisplatin 55-64 caspase 8 Homo sapiens 263-268 21128834-5 2011 Activation of caspase-3, caspase-8, and caspase-9 was observed within cisplatin-treated HEI-OC1 cells. Cisplatin 70-79 caspase 8 Homo sapiens 25-34 21801448-3 2011 We recently reported that the reconstitution of procaspase-8 is sufficient for sensitizing cisplatin- but not etoposide-induced apoptosis, in chemoresistant and caspase-8 deficient HOC313 head and neck squamous cell carcinoma (HNSCC) cells. Cisplatin 91-100 caspase 8 Homo sapiens 51-60 21487429-0 2011 Drug-induced caspase 8 upregulation sensitises cisplatin-resistant ovarian carcinoma cells to rhTRAIL-induced apoptosis. Cisplatin 47-56 caspase 8 Homo sapiens 13-22 21487429-6 2011 Pre-exposure of particularly CP70 to cisplatin resulted in strongly elevated caspase 8 protein and mRNA levels. Cisplatin 37-46 caspase 8 Homo sapiens 77-86 21487429-8 2011 Cisplatin-induced caspase 8 protein levels were essential for the rhTRAIL-sensitising effect as demonstrated using caspase 8 small-interfering RNA (siRNA) and caspase-8 overexpressing constructs. Cisplatin 0-9 caspase 8 Homo sapiens 18-27 21487429-8 2011 Cisplatin-induced caspase 8 protein levels were essential for the rhTRAIL-sensitising effect as demonstrated using caspase 8 small-interfering RNA (siRNA) and caspase-8 overexpressing constructs. Cisplatin 0-9 caspase 8 Homo sapiens 115-124 21487429-8 2011 Cisplatin-induced caspase 8 protein levels were essential for the rhTRAIL-sensitising effect as demonstrated using caspase 8 small-interfering RNA (siRNA) and caspase-8 overexpressing constructs. Cisplatin 0-9 caspase 8 Homo sapiens 159-168 21157427-6 2011 Finally, we demonstrate that this acetylation/phosphorylation signalling network controls SRSF2 accumulation as well as caspase-8 pre-mRNA splicing in response to cisplatin and determines whether cells undergo apoptosis or G(2)/M cell cycle arrest. Cisplatin 163-172 caspase 8 Homo sapiens 120-129 21216935-6 2011 Cisplatin and fisetin as single agents activated caspases-8 and -3 and caspases-9 and -7, respectively, whereas combination treatment activated all 4 caspases. Cisplatin 0-9 caspase 8 Homo sapiens 49-88 21214929-8 2011 RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2. Cisplatin 58-62 caspase 8 Homo sapiens 102-111 21052098-4 2011 We demonstrated that Ad-ING4 plus CDDP induced synergistic growth inhibition, enhanced apoptosis, and had an additive effect on upregulation of Fas, Bax, Bak, cleaved Bid, cleaved caspase-8, caspase-9, caspase-3 and cleaved PARP, and on downregulation of Bcl-2 and Bcl-X(L) in SMMC-7721 hepatocarcinoma cells. Cisplatin 34-38 caspase 8 Homo sapiens 180-189 21037225-4 2011 Here, we show that cisplatin or a more potent platinum(IV) complex LA-12 used in 20-fold lower concentration enhanced killing effects of TRAIL in human colon and prostate cancer cell lines via stimulation of caspase activity and overall apoptosis. Cisplatin 19-28 caspase 8 Homo sapiens 208-215 21364680-0 2010 Resistance to caspase-8 and -9 fragments in a malignant pleural mesothelioma cell line with acquired cisplatin-resistance. Cisplatin 101-110 caspase 8 Homo sapiens 14-30 20735432-8 2010 Mechanistically, PDCD4 significantly increased cisplatin-induced cleavage of caspase-3 and caspase-8, but had only a slight impact on caspase-9 cleavage and the expression of Bax and Bcl-2 in vitro and in vivo. Cisplatin 47-56 caspase 8 Homo sapiens 91-100 20735432-9 2010 A specific caspase-8 inhibitor, Z-ITED-FMK, attenuated cisplatin-induced apoptosis in PDCD4-overexpressing ovarian cancer cells. Cisplatin 55-64 caspase 8 Homo sapiens 11-20 21364680-4 2010 Acquisition of cisplatin-resistance resulted in basal fragmentation of caspase-8 and -9 without a concomitant increase in proteolytic activity, and there was an increased basal caspase-3/7 activity. Cisplatin 15-24 caspase 8 Homo sapiens 71-87 21364680-7 2010 We therefore concluded that in vitro acquisition of cisplatin-resistance rendered P31res1.2 cells resistant to caspase-8 and caspase-9 fragments and that cisplatin-induced, initiator-caspase independent caspase-3/7 activation was necessary to overcome this resistance. Cisplatin 52-61 caspase 8 Homo sapiens 111-120 19578756-5 2009 Both RT4 (grade I; wild-type p53) and T24 (grade III; mutant p53) cell types proved to be vulnerable to cisplatin apoptotic activity, albeit in a grade-dependent and drug dose-specific manner, as demonstrated by the proteolytic processing profiles of Caspase-8, Caspase-9, Caspase-3, and the Caspase repertoire characteristic substrates PARP and Lamin A/C, as well. Cisplatin 104-113 caspase 8 Homo sapiens 251-260 19852930-0 2009 Association of caspase-8 mutation with chemoresistance to cisplatin in HOC313 head and neck squamous cell carcinoma cells. Cisplatin 58-67 caspase 8 Homo sapiens 15-24 19852930-5 2009 Reconstitution of caspase-8 by stable transfection of wild-type caspase-8 sensitized the cells to cisplatin-, but not etoposide-induced apoptosis. Cisplatin 98-107 caspase 8 Homo sapiens 18-27 19852930-5 2009 Reconstitution of caspase-8 by stable transfection of wild-type caspase-8 sensitized the cells to cisplatin-, but not etoposide-induced apoptosis. Cisplatin 98-107 caspase 8 Homo sapiens 64-73 19852930-6 2009 Consistent with this, cisplatin, but not etoposide, induced TNF-alpha and TRAIL mRNA in caspase-8 reconstituted HOC313 cells, accompanied by activation of the reconstituted caspase-8 and its downstream caspase-3. Cisplatin 22-31 caspase 8 Homo sapiens 88-97 19852930-6 2009 Consistent with this, cisplatin, but not etoposide, induced TNF-alpha and TRAIL mRNA in caspase-8 reconstituted HOC313 cells, accompanied by activation of the reconstituted caspase-8 and its downstream caspase-3. Cisplatin 22-31 caspase 8 Homo sapiens 173-182 19852930-7 2009 These results indicate that the loss of caspase-8 plays an important role in acquisition of chemoresistance to cisplatin in HOC313 cells. Cisplatin 111-120 caspase 8 Homo sapiens 40-49 19625063-8 2009 Chemotherapy with doxorubicin or cisplatin (Ben Venue Laboratories, Bedford, Ohio) decreased the expression of the anti-apoptotic protein cFLIP(S) and increased caspase-8 cleavage, reversing TRAIL resistance in T24 cells. Cisplatin 33-42 caspase 8 Homo sapiens 161-170 19578756-5 2009 Both RT4 (grade I; wild-type p53) and T24 (grade III; mutant p53) cell types proved to be vulnerable to cisplatin apoptotic activity, albeit in a grade-dependent and drug dose-specific manner, as demonstrated by the proteolytic processing profiles of Caspase-8, Caspase-9, Caspase-3, and the Caspase repertoire characteristic substrates PARP and Lamin A/C, as well. Cisplatin 104-113 caspase 8 Homo sapiens 251-258 15604295-0 2004 Caspase inhibitors, but not c-Jun NH2-terminal kinase inhibitor treatment, prevent cisplatin-induced hearing loss. Cisplatin 83-92 caspase 8 Homo sapiens 0-7 19590723-0 2009 TRAIL-induced cell death and caspase-8 activation are inhibited by cisplatin but not carboplatin. Cisplatin 67-76 caspase 8 Homo sapiens 29-38 19590723-3 2009 However it has been recently reported that cisplatin may inhibit tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell death through inactivation of caspases. Cisplatin 43-52 caspase 8 Homo sapiens 172-180 19590723-8 2009 Whereas cisplatin inhibited caspase-8-mediated Bid cleavage, carboplatin had no effect on caspase-8 activity. Cisplatin 8-17 caspase 8 Homo sapiens 28-37 19276256-10 2009 Furthermore, the combination of lexatumumab and cisplatin significantly enhanced caspase-8 activity, Bid cleavage, up-regulation of Bax, cytochrome c release, and caspase-9, caspase-6, and caspase-3 activities. Cisplatin 48-57 caspase 8 Homo sapiens 81-90 19276256-14 2009 CONCLUSIONS: Cisplatin sensitizes solid cancer cells to lexatumumab-induced apoptosis by potentiation of the extrinsic and intrinsic apoptotic pathways that lead to amplification of caspase activation, particularly caspase-8, suggesting the combination treatment of solid cancers with cisplatin and lexatumumab might overcome their resistance. Cisplatin 13-22 caspase 8 Homo sapiens 215-224 17619073-7 2007 Similar to function way of SM, cDDP causes cancer cell apoptosis though caspase-8/caspase-3 and Bax/cytochrome c pathways, but the resistance to cDDP is correlated with Bcl-2 and Bcl-xL overexpression. Cisplatin 31-35 caspase 8 Homo sapiens 72-81 17452997-0 2007 Bcl-2 cleavages at two adjacent sites by different caspases promote cisplatin-induced apoptosis. Cisplatin 68-77 caspase 8 Homo sapiens 51-59 17452997-7 2007 These results indicate that Bcl-2 can be cleaved into two close fragments by different caspases during cisplatin-induced apoptosis, both of which contribute to the acceleration of apoptotic process. Cisplatin 103-112 caspase 8 Homo sapiens 87-95 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. Cisplatin 173-182 caspase 8 Homo sapiens 83-129 15863130-13 2005 Additionally, IFNgamma and cisplatin can increase sensitivity to anti-Fas in a subset of HPV-positive cervical cancer cell lines by upregulation of Fas and caspase-8 expression without major changes in p53 levels. Cisplatin 27-36 caspase 8 Homo sapiens 156-165 15386344-6 2004 Thus, activation of the Fas system is critical, which is in line with the finding that in sensitive cells, caspase-8 along with caspase-9 and -3 were activated by cDDP. Cisplatin 163-167 caspase 8 Homo sapiens 107-116 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. Cisplatin 124-133 caspase 8 Homo sapiens 51-60 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. Cisplatin 21-30 caspase 8 Homo sapiens 68-84 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. Cisplatin 48-57 caspase 8 Homo sapiens 93-109 17574045-11 2007 Our data indicate that the mitochondria-dependent feedback loop of the caspase activation cascade and the generation of ROS are both essential in mediating profound cytotoxicity and apoptosis of MPM cells treated with CDDP and sFasL. Cisplatin 218-222 caspase 8 Homo sapiens 71-78 17183590-6 2007 Activation of caspase-3, caspase-8, and caspase-9 was detected after treatment with cisplatin, and the cleavage of poly-(ADP)-ribose polymerase (PARP) was observed within cisplatin-treated HEI-OC1 cells. Cisplatin 84-93 caspase 8 Homo sapiens 25-34 17172403-5 2006 Significant activation of caspase-8, caspase-9, and caspase-3 was observed only in cells treated with cisplatin/Apo2L/TRAIL combination and not in those exposed to either agent alone. Cisplatin 102-111 caspase 8 Homo sapiens 26-35 17172403-7 2006 This observation strongly suggested that caspase-8 activation in cells treated with the cisplatin/Apo2L/TRAIL combination was secondary to the mitochondria-mediated amplification feedback loop and activation of the executioner caspase-3 was dependent on the recruitment of the intrinsic pathway characteristic of the type II cell. Cisplatin 88-97 caspase 8 Homo sapiens 41-50 17172403-9 2006 Cisplatin sensitizes esophageal cancer cells to Apo2L/TRAIL cytotoxicity by potentiation of the mitochondria-dependent death signaling pathway that leads to amplification of caspase activation, particularly caspase-8, by the feedback loop to efficiently induce apoptosis. Cisplatin 0-9 caspase 8 Homo sapiens 174-181 17172403-9 2006 Cisplatin sensitizes esophageal cancer cells to Apo2L/TRAIL cytotoxicity by potentiation of the mitochondria-dependent death signaling pathway that leads to amplification of caspase activation, particularly caspase-8, by the feedback loop to efficiently induce apoptosis. Cisplatin 0-9 caspase 8 Homo sapiens 207-216 16009487-3 2006 In T24 cells, cisplatin induce apoptosis and the activation of caspase-8, -9 and -3 and poly(ADP-ribose) polymerase cleavage. Cisplatin 14-23 caspase 8 Homo sapiens 63-83 16228292-5 2005 Cisplatin exerted same effects on cell viability and apoptosis in both cells, but released smaller amounts of cytochrome c while activated more caspase-8 in MCF-7/E6. Cisplatin 0-9 caspase 8 Homo sapiens 144-153 16044419-8 2005 Similarly upon treatment with cisplatin SiHa cells had more activation of caspases compared to that seen in HeLa cells under conditions of NF-kappaB inhibition by biological or chemical inhibitors. Cisplatin 30-39 caspase 8 Homo sapiens 74-82 15870947-4 2005 Cisplatin treatment induced the activation of caspase-8, -9 and -3 and the release of cytochrome c in apoptosis-sensitive Ma-46. Cisplatin 0-9 caspase 8 Homo sapiens 46-66 15289875-0 2004 Loss of caspase-8 activation pathway is a possible mechanism for CDDP resistance in human laryngeal squamous cell carcinoma, HEp-2 cells. Cisplatin 65-69 caspase 8 Homo sapiens 8-17 15336528-7 2004 Combinational treatment of SM and cisplatin synergistically enhanced caspase-8, -9, and -3 activities in A549 cells. Cisplatin 34-43 caspase 8 Homo sapiens 69-90 15258564-3 2004 Cisplatin significantly decreased FLIP protein level, induced cleavage of caspase-8 and caspase-3 and apoptosis in a concentration-dependent manner in cisplatin-sensitive but not -resistant cells. Cisplatin 0-9 caspase 8 Homo sapiens 74-83 15258564-3 2004 Cisplatin significantly decreased FLIP protein level, induced cleavage of caspase-8 and caspase-3 and apoptosis in a concentration-dependent manner in cisplatin-sensitive but not -resistant cells. Cisplatin 151-160 caspase 8 Homo sapiens 74-83 15258564-4 2004 While overexpression of FLIP-attenuated cisplatin-induced cleavage of caspase-8 and caspase-3 and apoptosis in chemosensitive cells, downregulation of FLIP in chemoresistant cells by siRNA increased apoptosis induced by cisplatin. Cisplatin 40-49 caspase 8 Homo sapiens 70-79 15289875-6 2004 CDDP activated the caspase-8 pathway through TNFR superfamily receptors such as Fas, but not caspase-9 in HeLa cells. Cisplatin 0-4 caspase 8 Homo sapiens 19-28 15289875-7 2004 On the other hand, the caspase-9 pathway was significantly activated in HEp-2 cells, although the activation of caspase-8 by CDDP was deficient. Cisplatin 125-129 caspase 8 Homo sapiens 112-121 15289875-8 2004 This different response to CDDP in caspase-8 activation was not related with the expression level of either Fas or FasL in these cells. Cisplatin 27-31 caspase 8 Homo sapiens 35-44 15289875-9 2004 We concluded from these results that loss of the caspase-8 activation pathway in HEp-2 cells was a possible mechanism for its resistance to CDDP-induced apoptosis. Cisplatin 140-144 caspase 8 Homo sapiens 49-58 15289875-10 2004 The caspase-8 pathway might play an important role in CDDP-induced apoptosis in HPV-positive human squamous cell carcinomas. Cisplatin 54-58 caspase 8 Homo sapiens 4-13 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. Cisplatin 75-84 caspase 8 Homo sapiens 232-241 15566959-8 2004 After 1 microM cisplatin treatment, Xrel3 had an anti-apoptotic effect, based on significantly lower levels of apoptotic proteins, including caspase-8, caspase-3 and p21. Cisplatin 15-24 caspase 8 Homo sapiens 141-150 15566959-10 2004 After 5 microM cisplatin treatment, expression of HeLa Xrel3 had an apoptotic effect, based on significantly increased expression of the cell cycle inhibitor p21 and apoptotic proteins, including cleaved PARP, caspase-8, and caspase-3. Cisplatin 15-24 caspase 8 Homo sapiens 210-219 12911332-1 2003 Cisplatin-selected cervix carcinoma HeLa cell lines induced less apoptosis, and weaker activation by cisplatin or Fas-activating antibody, of mitochondrial-associated caspase-9 and death receptor-mediated caspase-8 than did parental cells. Cisplatin 0-9 caspase 8 Homo sapiens 205-214 12911332-3 2003 Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines. Cisplatin 158-167 caspase 8 Homo sapiens 93-102 12911332-3 2003 Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines. Cisplatin 207-216 caspase 8 Homo sapiens 93-102 14519653-9 2003 CONCLUSIONS: The results presented here indicate that cisplatin inhibits c-FLIP protein expression and phosphorylation to restore TRAIL-induced caspase-8-initiated apoptosis in melanoma cells, thus providing a new combined therapeutic strategy for melanomas. Cisplatin 54-63 caspase 8 Homo sapiens 144-153 12912965-3 2003 The combination of TRAIL and cisplatin synergistically enhanced apoptotic death, caspase-8 and caspase-3 activation, as well as poly(ADP-ribose) polymerase cleavage. Cisplatin 29-38 caspase 8 Homo sapiens 81-90 12919886-8 2003 CDDP down-regulated c-FLIP, tending to lower the activation threshold required for TRAIL-induced caspase-8 activation. Cisplatin 0-4 caspase 8 Homo sapiens 97-106 12919886-9 2003 The CDDP-pretreated cells indeed demonstrated more increased TRAIL-mediated caspase-8 activation, loss of mitochondrial membrane potential (DeltaPsi(m)), and apoptosis than untreated cells. Cisplatin 4-8 caspase 8 Homo sapiens 76-85 12919886-11 2003 Both the increased caspase activation and mitochondrial dysfunction induced by combination of CDDP and TRAIL would contribute to enhanced apoptotic cell death. Cisplatin 94-98 caspase 8 Homo sapiens 19-26 12690107-5 2003 The proapoptotic effects of Ad-Bid were independent of p53 status and were augmented markedly by caspase-8 activators such as the DNA-damaging agent cisplatin. Cisplatin 149-158 caspase 8 Homo sapiens 97-106 12018840-5 2002 Cisplatin induced apoptosis with the cytochrome c release and caspase-3 activation in both wild-type and caspase-8-deficient JB-6 cells, while the Fas antibody induced these apoptotic events only in wild-type cells. Cisplatin 0-9 caspase 8 Homo sapiens 105-114 12543810-8 2003 In separate analysis of cells of early and late apoptotic stages, initiation of cisplatin-induced apoptosis appeared to be rather mediated by caspase-9 than by caspase-8. Cisplatin 80-89 caspase 8 Homo sapiens 160-169 12815464-4 2003 Cisplatin-induced apoptosis was efficiently blocked by caspase-8 inhibitor zIETD-fmk in Tera cells, but only partially in Tera-CP cells. Cisplatin 0-9 caspase 8 Homo sapiens 55-64 12815464-5 2003 In addition, cisplatin induced FADD and caspase-8 recruitment to the CD95 receptor in Tera cells, which was not noticed in Tera-CP cells. Cisplatin 13-22 caspase 8 Homo sapiens 40-49 12018840-10 2002 These data suggest that the cisplatin-induced apoptotic signal is initiated by the caspase-8-independent cytochrome c release, and the JNK activation protects cells from cisplatin-induced apoptosis via the metallothionein expression. Cisplatin 28-37 caspase 8 Homo sapiens 83-92 11859411-9 2002 Investigation of the mechanism by which a combination of drugs plus CD95 ligation can increase cell death showed that caspase-8 was activated in cells exposed to a combination of cisplatin and anti-CD95, but not in cells exposed to either agent alone. Cisplatin 179-188 caspase 8 Homo sapiens 118-127 11872042-9 2002 Of 1176 different human cDNA transcripts in cisplatin-treated TTSC-3, three genes (tumour necrosis factor receptor 1, caspase 8 and Apaf1), which are associated with apoptosis, were expressed markedly more than after saline injection. Cisplatin 44-53 caspase 8 Homo sapiens 118-127 11156422-3 2000 Using the NSCLC cell line NCI-H460 (H460), here, we studied the effect of stable expression of various caspase inhibitors on apoptosis induced by the anticancer drugs cisplatin, topotecan, and gemcitabine. Cisplatin 167-176 caspase 8 Homo sapiens 103-110 11703590-5 2001 RESULTS: The activation of initiator caspases-8, -9 and -2, and executioner caspase-3 began after eight hours of cisplatin treatment, thereafter markedly increased in a time (8 to 24 hours) and dose-dependent manner (0 to 200 micromol/L). Cisplatin 113-122 caspase 8 Homo sapiens 37-58 11566177-6 2001 Ac-LEHD-CHO, a caspase-9 inhibitor or Ac-IETD-CHO, a caspase-8 inhibitor, inhibited cisplatin-induced caspase-3 activation and apoptosis similarly in both cell lines. Cisplatin 84-93 caspase 8 Homo sapiens 53-62 11566177-13 2001 These results indicate that apoptosis and caspases are less induced in cisplatin-selected HeLa cells. Cisplatin 71-80 caspase 8 Homo sapiens 42-50 34299199-6 2021 The results showed that ruthenium compounds break partially or completely the cisplatin resistance by activating the caspase 8-dependent apoptosis pathway and loss of mitochondrial membrane potential. Cisplatin 78-87 caspase 8 Homo sapiens 117-126 35070983-14 2021 Furthermore, quercetin combined with cisplatin downregulated the expression of EGFR, MYC, CCND1, and ERBB2 proteins and upregulated CASP8 expression in HeLa and SiHa cells. Cisplatin 37-46 caspase 8 Homo sapiens 132-137 10663637-0 2000 Cisplatin (CDDP) specifically induces apoptosis via sequential activation of caspase-8, -3 and -6 in osteosarcoma. Cisplatin 0-9 caspase 8 Homo sapiens 77-97 10663637-0 2000 Cisplatin (CDDP) specifically induces apoptosis via sequential activation of caspase-8, -3 and -6 in osteosarcoma. Cisplatin 11-15 caspase 8 Homo sapiens 77-97 10663637-20 2000 It also demonstrates that caspase-8 is a key molecule in the earliest stage of the signaling pathway of CDDP-induced apoptosis of HOS cells, and caspase-3 works downstream of caspase-8. Cisplatin 104-108 caspase 8 Homo sapiens 26-35 10663637-20 2000 It also demonstrates that caspase-8 is a key molecule in the earliest stage of the signaling pathway of CDDP-induced apoptosis of HOS cells, and caspase-3 works downstream of caspase-8. Cisplatin 104-108 caspase 8 Homo sapiens 175-184 34994335-10 2022 These compounds combined with cisplatin caused upregulation in the pro-apoptotic Bax, Bid, caspase-3, caspase-8, caspase-9, Fas, and p53 gene expressions while downregulating anti-apoptotic DFFA, NFkB1, and Bcl2 gene expressions. Cisplatin 30-39 caspase 8 Homo sapiens 102-111