PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19387079-6 2009 Vorinostat increased p53 expression and activated caspases -8, -9 and -3, whereas caspase inhibition abrogated vorinostat-induced apoptosis. Vorinostat 0-10 caspase 8 Homo sapiens 50-72 19737941-4 2009 Western blotting showed suberoylanilide hydroxamic acid increased Fas, Fas ligand, DR4, and DR5 protein expression and activated caspase-8 and caspase-9. Vorinostat 24-55 caspase 8 Homo sapiens 129-138 19597472-4 2009 HDACI, for example, valproic acid (VA), suberoylanilide hydroxamic acid (SAHA) and MS-275, cooperate with IFN-gamma to upregulate caspase-8 in cancer cells lacking caspase-8, thereby restoring sensitivity to TRAIL-induced apoptosis. Vorinostat 40-71 caspase 8 Homo sapiens 130-139 19597472-4 2009 HDACI, for example, valproic acid (VA), suberoylanilide hydroxamic acid (SAHA) and MS-275, cooperate with IFN-gamma to upregulate caspase-8 in cancer cells lacking caspase-8, thereby restoring sensitivity to TRAIL-induced apoptosis. Vorinostat 73-77 caspase 8 Homo sapiens 130-139 18787411-11 2008 Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival). Vorinostat 19-29 caspase 8 Homo sapiens 175-184 18787411-3 2008 Low doses of sorafenib and vorinostat, but not the individual agents, caused an acidic sphingomyelinase and fumonisin B1-dependent increase in CD95 surface levels and CD95 association with caspase 8. Vorinostat 27-37 caspase 8 Homo sapiens 189-198 15897598-4 2005 In these models, both SAHA and m-carboxycinnamic acid bis-hydroxamide induced growth arrest and caspase-mediated apoptosis and increased p21 protein levels, retinoblastoma hypophosphorylation, BH3-interacting domain death agonist cleavage, Bax up-regulation, down-regulation of Bcl-2, A1, and Bcl-x(L) expression, and cleavage of poly(ADP-ribose) polymerase and caspase-8, -9, -3, -7, and -2. Vorinostat 22-26 caspase 8 Homo sapiens 362-391 18636153-6 2008 In addition, SAHA up-regulated the death receptor DR5, inducing the activation of caspase-8 with the consequent cleavage of Bid. Vorinostat 13-17 caspase 8 Homo sapiens 82-91 17351739-3 2007 In HepG2 cells SAHA induced the extrinsic apoptotic pathway, increasing the expression of both FasL and FasL receptor and causing the activation of caspase-8. Vorinostat 15-19 caspase 8 Homo sapiens 148-157 16550602-6 2006 The sensitization of these cells by SAHA was accompanied by activation of caspase 8, caspase 9 and caspase 3 and was concomitant with Bid and PARP cleavage. Vorinostat 36-40 caspase 8 Homo sapiens 74-83 18765530-7 2008 Sorafenib and vorinostat treatment increased surface levels of CD95 and CD95 association with caspase-8. Vorinostat 14-24 caspase 8 Homo sapiens 94-103 18065490-6 2007 Pharmacologic or genetic inhibition of caspase-8 reduced flavopiridol toxicity, but abolished killing by vorinostat and cell death caused by the vorinostat/flavopiridol regimen. Vorinostat 105-115 caspase 8 Homo sapiens 39-48 18065490-6 2007 Pharmacologic or genetic inhibition of caspase-8 reduced flavopiridol toxicity, but abolished killing by vorinostat and cell death caused by the vorinostat/flavopiridol regimen. Vorinostat 145-155 caspase 8 Homo sapiens 39-48 18025281-7 2007 SAHA also activated the extrinsic apoptosis pathway, including increased Fas and Fas ligand (FasL) expression, activation of caspase-8, and cleavage of Bid. Vorinostat 0-4 caspase 8 Homo sapiens 125-134 28099148-11 2017 In conclusion, SAHA inhibited the growth of lung cancer cells via a G2/M phase arrest and caspase-dependent apoptosis. Vorinostat 15-19 caspase 8 Homo sapiens 90-97 27863490-6 2016 Furthermore, at high concentrations (more than 5 muM), SAHA triggered apoptosis of GSCs accompanied by increases in both activation of caspase 8- and caspase 9-mediated pathways. Vorinostat 55-59 caspase 8 Homo sapiens 135-144 24236158-6 2013 In contrast, SAHA increased expression of Caspase-3, p21 and p53 mRNA, and upregulated acetyl-Histones H3 and H4, Caspase-8, and p53 proteins. Vorinostat 13-17 caspase 8 Homo sapiens 114-123 24651472-1 2014 We have recently demonstrated that histone deacetylase inhibitor, Vorinostat, applied as a single therapy or in combination with caspase-8 downregulation exhibits high anti-tumoral activity on endometrial carcinoma cell lines. Vorinostat 66-76 caspase 8 Homo sapiens 129-138 27474150-6 2016 The clinically relevant histone deacetylase (HDAC) inhibitors vorinostat and entinostat were subsequently found to sensitize a subset of NSCLC cell lines to IR in a manner that was dependent on their ability to suppress FLIP expression and promote activation of caspase-8. Vorinostat 62-72 caspase 8 Homo sapiens 262-271 23868066-9 2013 Although treatment with SMC in the presence of TNFalpha promoted interaction between caspase 8 and the necrosis-promoting RIPK1, the cell death induced by combined treatment with SAHA and SMC was apoptotic and mediated by caspase 8. Vorinostat 179-183 caspase 8 Homo sapiens 222-231 23590818-4 2013 Vorinostat-induced the activation of caspase-8 and -9, the initiators caspases of the extrinsic and the intrinsic apoptotic pathways, respectively. Vorinostat 0-10 caspase 8 Homo sapiens 37-53 23590818-4 2013 Vorinostat-induced the activation of caspase-8 and -9, the initiators caspases of the extrinsic and the intrinsic apoptotic pathways, respectively. Vorinostat 0-10 caspase 8 Homo sapiens 70-78 23590818-8 2013 To further investigate the role of extrinsic apoptotic pathway in Vorinostat-induced apoptosis, we performed an shRNA-mediated knock-down of caspase-8. Vorinostat 66-76 caspase 8 Homo sapiens 141-150 23086637-10 2012 CONCLUSION: Combining HDAC inhibitor SAHA with imatinib can kill CML cells synergistically by inhibiting cell growth and inducing apoptosis, which is associated with activation of Caspase pathway and regulation of anti-apoptotic proteins. Vorinostat 37-41 caspase 8 Homo sapiens 180-187 22322857-4 2012 Using in vitro and in vivo colorectal cancer models, we further demonstrated that SAHA-induced apoptosis is dependant on FLIP downregulation and caspase 8 activation. Vorinostat 82-86 caspase 8 Homo sapiens 145-154 22154545-0 2012 Vorinostat/SAHA-induced apoptosis in malignant mesothelioma is FLIP/caspase 8-dependent and HR23B-independent. Vorinostat 0-10 caspase 8 Homo sapiens 68-77 22154545-0 2012 Vorinostat/SAHA-induced apoptosis in malignant mesothelioma is FLIP/caspase 8-dependent and HR23B-independent. Vorinostat 11-15 caspase 8 Homo sapiens 68-77