PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29928452-0 2018 Luteolin and sorafenib combination kills human hepatocellular carcinoma cells through apoptosis potentiation and JNK activation. Sorafenib 13-22 mitogen-activated protein kinase 8 Homo sapiens 113-116 34332981-0 2021 Dichloroacetate enhances the anti-tumor effect of sorafenib via modulating the ROS-JNK-Mcl-1 pathway in liver cancer cells. Sorafenib 50-59 mitogen-activated protein kinase 8 Homo sapiens 83-86 34332981-9 2021 Furthermore, we found that the ROS-JNK pathway was obviously activated in the DCA combined sorafenib group. Sorafenib 91-100 mitogen-activated protein kinase 8 Homo sapiens 35-38 34332981-11 2021 Antioxidant NAC could alleviate the synergetic effects of DCA and sorafenib on ROS generation, JNK activation, Mcl-1 degradation, and cell apoptosis. Sorafenib 66-75 mitogen-activated protein kinase 8 Homo sapiens 95-98 34332981-14 2021 These findings indicate that DCA enhances the anti-tumor effect of sorafenib via the ROS-JNK-Mcl-1 pathway in liver cancer cells. Sorafenib 67-76 mitogen-activated protein kinase 8 Homo sapiens 89-92 35129807-0 2022 Zinc supplementation ameliorates sorafenib-induced cognitive impairment through ROS/JNK signaling pathway. Sorafenib 33-42 mitogen-activated protein kinase 8 Homo sapiens 84-87 32636042-0 2020 Retraction notice to "Cytokine augments the sorafenib-induced apoptosis in Huh7 liver cancer cell by inducing mitochondrial fragmentation and activating MAPK-JNK signalling pathway" [Biomed. Sorafenib 44-53 mitogen-activated protein kinase 8 Homo sapiens 158-161 30476722-0 2019 Cytokine augments the sorafenib-induced apoptosis in Huh7 liver cancer cell by inducing mitochondrial fragmentation and activating MAPK-JNK signalling pathway. Sorafenib 22-31 mitogen-activated protein kinase 8 Homo sapiens 136-139 30476722-10 2019 Blockade of the JNK signalling pathway and/or knockdown of TAZ could abrogate the inhibitor effects of IL-2/sorafenib on liver cancer survival, growth and mobility. Sorafenib 108-117 mitogen-activated protein kinase 8 Homo sapiens 16-19 30476722-11 2019 Collectively, these data indicated that IL-2 supplementation could further augment the anti-cancer effectiveness of sorafenib via activating mitochondrial fragmentation in a manner dependent on MAPK-JNK signalling pathway and TAZ protein. Sorafenib 116-125 mitogen-activated protein kinase 8 Homo sapiens 199-202 34767735-12 2021 In summary, we infer that the RABL2A-CCDC34 axis plays an important role in mediating p38/MAPK and JNK/MAPK signaling, thereby contributing to acquired sorafenib resistance in HCC. Sorafenib 152-161 mitogen-activated protein kinase 8 Homo sapiens 99-102 33667419-6 2021 Knockdown simulations identified AP1, ASK1, JNK, MEK47, p53, and ROS as positive functional regulators of sorafenib-induced apoptosis of cardiomyocytes. Sorafenib 106-115 mitogen-activated protein kinase 8 Homo sapiens 44-47 30187994-0 2018 Synergistic antimetastatic effect of cotreatment with licochalcone A and sorafenib on human hepatocellular carcinoma cells through the inactivation of MKK4/JNK and uPA expression. Sorafenib 73-82 mitogen-activated protein kinase 8 Homo sapiens 156-159 30459526-0 2018 IL-2 augments the sorafenib-induced apoptosis in liver cancer by promoting mitochondrial fission and activating the JNK/TAZ pathway. Sorafenib 18-27 mitogen-activated protein kinase 8 Homo sapiens 116-119 30459526-12 2018 Finally, we found that IL-2/sorafenib regulated mitochondrial fission via the JNK-TAZ pathways; blockade of the JNK-TAZ pathways abrogated the inhibitory effects of L-2/sorafenib on cancer survival, growth and mobility. Sorafenib 28-37 mitogen-activated protein kinase 8 Homo sapiens 78-81 30459526-12 2018 Finally, we found that IL-2/sorafenib regulated mitochondrial fission via the JNK-TAZ pathways; blockade of the JNK-TAZ pathways abrogated the inhibitory effects of L-2/sorafenib on cancer survival, growth and mobility. Sorafenib 169-178 mitogen-activated protein kinase 8 Homo sapiens 78-81 30459526-12 2018 Finally, we found that IL-2/sorafenib regulated mitochondrial fission via the JNK-TAZ pathways; blockade of the JNK-TAZ pathways abrogated the inhibitory effects of L-2/sorafenib on cancer survival, growth and mobility. Sorafenib 169-178 mitogen-activated protein kinase 8 Homo sapiens 112-115 30459526-13 2018 Conclusions: Altogether, these data strongly suggest that additional supplementation with IL-2 enhances the anti-tumour activity of sorafenib by promoting the JNK-TAZ-mitochondrial fission axis. Sorafenib 132-141 mitogen-activated protein kinase 8 Homo sapiens 159-162 30443188-3 2018 In our study, we evaluated effect of quisinostat alone and in combination with sorafenib in HCC cells via inducing G0/G1 phase arrest through PI3K/AKT/p21 pathway and apoptosis by JNK/c-Jun/caspase3 pathway in vitro and in vivo. Sorafenib 79-88 mitogen-activated protein kinase 8 Homo sapiens 180-183 29864454-0 2018 RASSF6-mediated inhibition of Mcl-1 through JNK activation improves the anti-tumor effects of sorafenib in renal cell carcinoma. Sorafenib 94-103 mitogen-activated protein kinase 8 Homo sapiens 44-47 29864454-6 2018 Suppression of the JNK pathway can partially restore Mcl-1 expression and sorafenib resistance. Sorafenib 74-83 mitogen-activated protein kinase 8 Homo sapiens 19-22 29864454-7 2018 Together, these findings suggest that RASSF6 inhibits sorafenib resistance by repressing Mcl-1 through the JNK-dependent pathway. Sorafenib 54-63 mitogen-activated protein kinase 8 Homo sapiens 107-110 29928452-9 2018 Thus, sorafenib and luteolin combination synergistically kills HCC cells through JNK-mediated apoptosis, and luteolin may be an ideal candidate for increasing the activity of sorafenib in HCC therapy. Sorafenib 6-15 mitogen-activated protein kinase 8 Homo sapiens 81-84 30132846-8 2018 In conclusion, the early sorafenib-induced ER stress and regulation of JNK and AMPK-dependent signaling were related to the induction of survival autophagic process. Sorafenib 25-34 mitogen-activated protein kinase 8 Homo sapiens 71-74 28055301-7 2017 Specifically, our results indicate that sorafenib triggers a mechanistic MAPK/JNK-dependent early protective autophagic response in EC cells, providing an adaptive response to therapeutic stress. Sorafenib 40-49 mitogen-activated protein kinase 8 Homo sapiens 78-81 29033791-10 2017 We further demonstrate that the multikinase inhibitor sorafenib completely prevents JNK activation, while providing only moderate hair cell protection. Sorafenib 54-63 mitogen-activated protein kinase 8 Homo sapiens 84-87 28178378-5 2017 Furthermore, FACS and TUNEL assay confirmed that melatonin synergistically augmented the sorafenib-induced apoptosis after 48 hours incubation, which was in accordance with the activation of caspase-3 and the JNK/c-jun pathway. Sorafenib 89-98 mitogen-activated protein kinase 8 Homo sapiens 209-212 28178378-6 2017 Inhibition of JNK/c-jun pathway with its inhibitor SP600125 reversed the phosphorylation of c-jun and the activation of caspase-3 induced by co-treatment of HuH-7 cells with melatonin and sorafenib in a dose-dependent manner. Sorafenib 188-197 mitogen-activated protein kinase 8 Homo sapiens 14-17 28178378-0 2017 Melatonin promotes sorafenib-induced apoptosis through synergistic activation of JNK/c-jun pathway in human hepatocellular carcinoma. Sorafenib 19-28 mitogen-activated protein kinase 8 Homo sapiens 81-84 25245054-0 2014 Metformin inhibits the invasion of human hepatocellular carcinoma cells and enhances the chemosensitivity to sorafenib through a downregulation of the ERK/JNK-mediated NF-kappaB-dependent pathway that reduces uPA and MMP-9 expression. Sorafenib 109-118 mitogen-activated protein kinase 8 Homo sapiens 155-158 26964667-9 2016 p-c-Jun may act as a biomarker for predicting responses of sorafenib treatment, thus advocating targeting of JNK/c-Jun signaling as an optimal therapeutic strategy in a subset of HCC. Sorafenib 59-68 mitogen-activated protein kinase 8 Homo sapiens 109-112 26629768-0 2016 Sorafenib induces autophagic cell death and apoptosis in hepatic stellate cell through the JNK and Akt signaling pathways. Sorafenib 0-9 mitogen-activated protein kinase 8 Homo sapiens 91-94 26629768-12 2016 Finally, sorafenib induced programmed cell death by attenuation and activation of Akt/mTOR/p70S6K and JNK signaling. Sorafenib 9-18 mitogen-activated protein kinase 8 Homo sapiens 102-105 26460271-0 2015 Sorafenib inhibits cancer side population cells by targeting c-Jun N-terminal kinase signaling. Sorafenib 0-9 mitogen-activated protein kinase 8 Homo sapiens 61-84 26460271-5 2015 Sorafenib and 5-FU treatment decreased growth rates in Huh7 and Huh-BAT cells; however, the treatments exerted different effects in SP cells and on the expression levels of JNK signaling molecules. Sorafenib 0-9 mitogen-activated protein kinase 8 Homo sapiens 173-176 26460271-7 2015 By contrast, sorafenib decreased the SP cell number and downregulated the expression of JNK signaling molecules. Sorafenib 13-22 mitogen-activated protein kinase 8 Homo sapiens 88-91 26460271-9 2015 These results indicate that sorafenib exerted anticancer effects in HCC and SP cells by targeting JNK signaling. Sorafenib 28-37 mitogen-activated protein kinase 8 Homo sapiens 98-101 26517516-0 2015 Identification of the beta-catenin/JNK/prothymosin-alpha axis as a novel target of sorafenib in hepatocellular carcinoma cells. Sorafenib 83-92 mitogen-activated protein kinase 8 Homo sapiens 35-38 25683251-8 2015 In the combination treatment using ATRA and sorafenib, increased apoptosis, followed by the activation of p38 MAPK and JNK, the upregulation and translocation of Bax to mitochondria, and the activation of caspase-3, was observed. Sorafenib 44-53 mitogen-activated protein kinase 8 Homo sapiens 119-122 16985072-0 2006 Cytotoxic synergy between the multikinase inhibitor sorafenib and the proteasome inhibitor bortezomib in vitro: induction of apoptosis through Akt and c-Jun NH2-terminal kinase pathways. Sorafenib 52-61 mitogen-activated protein kinase 8 Homo sapiens 151-176 24402682-0 2014 ROS-mediated JNK/p38-MAPK activation regulates Bax translocation in Sorafenib-induced apoptosis of EBV-transformed B cells. Sorafenib 68-77 mitogen-activated protein kinase 8 Homo sapiens 13-16 24170769-0 2014 Sorafenib suppresses JNK-dependent apoptosis through inhibition of ZAK. Sorafenib 0-9 mitogen-activated protein kinase 8 Homo sapiens 21-24 24170769-4 2014 Here, we report that sorafenib suppresses UV-induced apoptosis specifically by inhibiting c-jun-NH(2)-kinase (JNK) activation through the off-target inhibition of leucine zipper and sterile alpha motif-containing kinase (ZAK). Sorafenib 21-30 mitogen-activated protein kinase 8 Homo sapiens 90-108 24170769-4 2014 Here, we report that sorafenib suppresses UV-induced apoptosis specifically by inhibiting c-jun-NH(2)-kinase (JNK) activation through the off-target inhibition of leucine zipper and sterile alpha motif-containing kinase (ZAK). Sorafenib 21-30 mitogen-activated protein kinase 8 Homo sapiens 110-113 24170769-5 2014 Our results implicate suppression of JNK signaling, independent of the ERK pathway, as an additional mechanism of adverse effects of sorafenib. Sorafenib 133-142 mitogen-activated protein kinase 8 Homo sapiens 37-40 22596232-0 2012 Activation of JNK and high expression level of CD133 predict a poor response to sorafenib in hepatocellular carcinoma. Sorafenib 80-89 mitogen-activated protein kinase 8 Homo sapiens 14-17 22596232-5 2012 RESULTS: In patients treated with sorafenib, the expression of phospho-c-Jun in HCC, as a read out of JNK activity, was significantly higher (P<0.001) in the non-responder group than in the responder group. Sorafenib 34-43 mitogen-activated protein kinase 8 Homo sapiens 102-105 22596232-10 2012 In conclusion, JNK activation was positively correlated with CD133 expression level and inversely correlated with the therapeutic response to sorafenib, suggesting that JNK activity may be considered as a new predictive biomarker for response to sorafenib treatment. Sorafenib 142-151 mitogen-activated protein kinase 8 Homo sapiens 15-18 22596232-10 2012 In conclusion, JNK activation was positively correlated with CD133 expression level and inversely correlated with the therapeutic response to sorafenib, suggesting that JNK activity may be considered as a new predictive biomarker for response to sorafenib treatment. Sorafenib 142-151 mitogen-activated protein kinase 8 Homo sapiens 169-172 22596232-10 2012 In conclusion, JNK activation was positively correlated with CD133 expression level and inversely correlated with the therapeutic response to sorafenib, suggesting that JNK activity may be considered as a new predictive biomarker for response to sorafenib treatment. Sorafenib 246-255 mitogen-activated protein kinase 8 Homo sapiens 15-18 22596232-10 2012 In conclusion, JNK activation was positively correlated with CD133 expression level and inversely correlated with the therapeutic response to sorafenib, suggesting that JNK activity may be considered as a new predictive biomarker for response to sorafenib treatment. Sorafenib 246-255 mitogen-activated protein kinase 8 Homo sapiens 169-172 21062976-6 2010 However, c-Jun NH2-terminal kinase (JNK) kinase activation occurred preferentially in sorafenib-sensitive cells. Sorafenib 86-95 mitogen-activated protein kinase 8 Homo sapiens 9-34 21062976-6 2010 However, c-Jun NH2-terminal kinase (JNK) kinase activation occurred preferentially in sorafenib-sensitive cells. Sorafenib 86-95 mitogen-activated protein kinase 8 Homo sapiens 36-39 21062976-7 2010 Small interfering RNA-mediated knockdown of GADD45betaor JNK kinase limited the proapoptotic effects of sorafenib in sorafenib-sensitive cells. Sorafenib 104-113 mitogen-activated protein kinase 8 Homo sapiens 57-60 21062976-7 2010 Small interfering RNA-mediated knockdown of GADD45betaor JNK kinase limited the proapoptotic effects of sorafenib in sorafenib-sensitive cells. Sorafenib 117-126 mitogen-activated protein kinase 8 Homo sapiens 57-60 24726537-7 2014 Overall, we discovered that beta1 integrin and its downstream effector JNK mediate sorafenib resistance during tumor stiffening. Sorafenib 83-92 mitogen-activated protein kinase 8 Homo sapiens 71-74 20301194-9 2010 Vitamin K1 plus Sorafenib combination also resulted in elevated levels of activated c-Jun N-terminal kinase (JNK) and its substrates c-Jun and FasL. Sorafenib 16-25 mitogen-activated protein kinase 8 Homo sapiens 84-107 20301194-9 2010 Vitamin K1 plus Sorafenib combination also resulted in elevated levels of activated c-Jun N-terminal kinase (JNK) and its substrates c-Jun and FasL. Sorafenib 16-25 mitogen-activated protein kinase 8 Homo sapiens 109-112 20301194-11 2010 Thus, combination VK1 plus Sorafenib strongly induced growth inhibition and apoptosis in pancreas cancer cells, involving both inhibition of the RAF/MEK/ERK pathway as well as activation of the JNK, c-Jun and FasL apoptotic pathway. Sorafenib 27-36 mitogen-activated protein kinase 8 Homo sapiens 194-197 16985072-7 2006 These findings show that sorafenib interacts synergistically with bortezomib to induce apoptosis in a broad spectrum of neoplastic cell lines and show an important role for the Akt and JNK pathways in mediating synergism. Sorafenib 25-34 mitogen-activated protein kinase 8 Homo sapiens 185-188