PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29137334-0 2017 The coffee diterpene kahweol enhances sensitivity to sorafenib in human renal carcinoma Caki cells through down-regulation of Mcl-1 and c-FLIP expression. Sorafenib 53-62 CASP8 and FADD like apoptosis regulator Homo sapiens 136-142 30066934-0 2018 Inhibition of cFLIP overcomes acquired resistance to sorafenib via reducing ER stress-related autophagy in hepatocellular carcinoma. Sorafenib 53-62 CASP8 and FADD like apoptosis regulator Homo sapiens 14-19 30066934-12 2018 The knockdown of cFLIP reversed the acquired sorafenib resistance by activating caspase-8 and inhibiting activated ERS in the sorafenib-resistant HCC cells. Sorafenib 45-54 CASP8 and FADD like apoptosis regulator Homo sapiens 17-22 30066934-12 2018 The knockdown of cFLIP reversed the acquired sorafenib resistance by activating caspase-8 and inhibiting activated ERS in the sorafenib-resistant HCC cells. Sorafenib 126-135 CASP8 and FADD like apoptosis regulator Homo sapiens 17-22 30066934-14 2018 In conclusion, cFLIP was identified as a potential target for overcoming the acquired sorafenib resistance in HCC. Sorafenib 86-95 CASP8 and FADD like apoptosis regulator Homo sapiens 15-20 29545419-0 2018 Correction: The Multikinase Inhibitor Sorafenib Potentiates TRAIL Lethality in Human Leukemia Cells in Association with Mcl-1 and cFLIPL Down-regulation. Sorafenib 38-47 CASP8 and FADD like apoptosis regulator Homo sapiens 130-136 29137334-5 2017 Combined treatment with sorafenib and kahweol induced down-regulation of Mcl-1 and c-FLIP expression. Sorafenib 24-33 CASP8 and FADD like apoptosis regulator Homo sapiens 83-89 29137334-8 2017 Interestingly, combined treatment with sorafenib and kahweol induced apoptotic cell death in c-FLIP overexpressed cells. Sorafenib 39-48 CASP8 and FADD like apoptosis regulator Homo sapiens 93-99 18765530-5 2008 However, 24 h after exposure, sorafenib- and vorinostat-treated cells exhibited markedly diminished expression of c-FLIP-s, full-length BID, BCL-2, BCL-XL, MCL-1, XIAP, increased expression of BIM, and increased activation of BAX, BAK, and BAD. Sorafenib 30-39 CASP8 and FADD like apoptosis regulator Homo sapiens 114-120 20038816-7 2009 Within 3 h of sorafenib treatment, a number of known pro-survival molecules were dephosphorylated and/or downregulated in expression including MCL-1(L), c-FLIP(L), survivin and cIAP(1). Sorafenib 14-23 CASP8 and FADD like apoptosis regulator Homo sapiens 153-162 20071162-6 2010 Sorafenib treatment correlated with a downregulation of both FLICE-Inhibitory Protein (FLIP) and myeloid cell leukaemia-1 (Mcl-1), caused by a proteasomal degradation of both proteins. Sorafenib 0-9 CASP8 and FADD like apoptosis regulator Homo sapiens 61-85 19483104-3 2009 In SW480 cells, sorafenib + vorinostat increased CD95 plasma membrane levels and promoted death-inducing signal complex (DISC) formation, and drug toxicity was blocked by knockdown of CD95 or overexpression of cellular FLICE-like inhibitory protein (c-FLIP-s). Sorafenib 16-25 CASP8 and FADD like apoptosis regulator Homo sapiens 210-248 19483104-3 2009 In SW480 cells, sorafenib + vorinostat increased CD95 plasma membrane levels and promoted death-inducing signal complex (DISC) formation, and drug toxicity was blocked by knockdown of CD95 or overexpression of cellular FLICE-like inhibitory protein (c-FLIP-s). Sorafenib 16-25 CASP8 and FADD like apoptosis regulator Homo sapiens 250-256 19483105-3 2009 Overexpression of cellular FLICE-like inhibitory protein (c-FLIP-s) or knockdown of CD95 suppressed the lethality of the sorafenib/HDACI combination (sorafenib + HDACI). Sorafenib 121-130 CASP8 and FADD like apoptosis regulator Homo sapiens 18-56 19483105-3 2009 Overexpression of cellular FLICE-like inhibitory protein (c-FLIP-s) or knockdown of CD95 suppressed the lethality of the sorafenib/HDACI combination (sorafenib + HDACI). Sorafenib 121-130 CASP8 and FADD like apoptosis regulator Homo sapiens 58-64 19483105-3 2009 Overexpression of cellular FLICE-like inhibitory protein (c-FLIP-s) or knockdown of CD95 suppressed the lethality of the sorafenib/HDACI combination (sorafenib + HDACI). Sorafenib 150-159 CASP8 and FADD like apoptosis regulator Homo sapiens 18-56 19483105-3 2009 Overexpression of cellular FLICE-like inhibitory protein (c-FLIP-s) or knockdown of CD95 suppressed the lethality of the sorafenib/HDACI combination (sorafenib + HDACI). Sorafenib 150-159 CASP8 and FADD like apoptosis regulator Homo sapiens 58-64 18765530-6 2008 Expression of eIF2alpha S51A blocked sorafenib- and vorinostat-induced suppression of c-FLIP-s levels and overexpression of c-FLIP-s abolished lethality. Sorafenib 37-46 CASP8 and FADD like apoptosis regulator Homo sapiens 86-92 18765530-9 2008 CONCLUSIONS: These data show that combined exposure of epithelial tumor cell types to sorafenib and vorinostat diminishes expression of multiple antiapoptotic proteins and promotes activation of the CD95 extrinsic apoptotic and the lysosomal protease pathways, and that suppression of c-FLIP-s expression represents a critical event in transduction of the proapoptotic signals from CD95 to promote mitochondrial dysfunction and death. Sorafenib 86-95 CASP8 and FADD like apoptosis regulator Homo sapiens 285-291 17909059-0 2007 The multikinase inhibitor sorafenib potentiates TRAIL lethality in human leukemia cells in association with Mcl-1 and cFLIPL down-regulation. Sorafenib 26-35 CASP8 and FADD like apoptosis regulator Homo sapiens 118-124 17909059-9 2007 Sorafenib also down-regulated cFLIP(L), most likely through a translational mechanism, in association with diminished eIF4E phosphorylation, whereas ectopic expression of cFLIP(L) significantly reduced sorafenib/TRAIL lethality. Sorafenib 0-9 CASP8 and FADD like apoptosis regulator Homo sapiens 30-38 17909059-9 2007 Sorafenib also down-regulated cFLIP(L), most likely through a translational mechanism, in association with diminished eIF4E phosphorylation, whereas ectopic expression of cFLIP(L) significantly reduced sorafenib/TRAIL lethality. Sorafenib 202-211 CASP8 and FADD like apoptosis regulator Homo sapiens 171-179 17909059-10 2007 Together, these results suggest that in human leukemia cells, sorafenib potentiates TRAIL-induced lethality by down-regulating Mcl-1 and cFLIP(L), events that cooperate to engage the intrinsic and extrinsic apoptotic cascades, culminating in pronounced mitochondrial injury and apoptosis. Sorafenib 62-71 CASP8 and FADD like apoptosis regulator Homo sapiens 137-145