PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20950443-0 2010 The multikinase inhibitor Sorafenib displays significant antiproliferative effects and induces apoptosis via caspase 3, 7 and PARP in B- and T-lymphoblastic cells. Sorafenib 26-35 caspase 3 Homo sapiens 109-118 22176637-3 2012 METHODS: Cell viability and apoptosis were evaluated in two HB cell lines (HUH6 and HepT1) after treatment with sorafenib using MTT and Caspase 3 activation assay. Sorafenib 112-121 caspase 3 Homo sapiens 136-145 20197401-12 2010 Because the BH3-only Bim protein is a potent inducer of mitochondrial apoptosis, Bim knockdown was shown to attenuate caspase-3, caspase-9 cleavage, and Bax/Bak activation by sorafenib plus TRAIL. Sorafenib 175-184 caspase 3 Homo sapiens 118-127 20473320-5 2010 Sorafenib induced caspase-3 cleavage and the mitochondrial release of cytochrome c. Sorafenib 0-9 caspase 3 Homo sapiens 18-27 22993610-9 2010 The expression levels of cyclin D1 decreased and the cleavage of caspase-3 was noted in the serum-free media with sorafenib. Sorafenib 114-123 caspase 3 Homo sapiens 65-74 35241510-11 2022 Compared to sorafenib or bufalin treatment alone, the combination treatment resulted in lower Bcl-2 expression but higher Bax, Bad, APAF-1, caspase-3, and caspase-9. Sorafenib 12-21 caspase 3 Homo sapiens 140-149 19366808-5 2009 It was further revealed that sorafenib activates Bax and caspase-3 and reduces mitochondrial membrane potential specifically in BCR/ABL-driven cells. Sorafenib 29-38 caspase 3 Homo sapiens 57-66 35245519-0 2022 Antitumor effects of rhamnazinon sorafenib-treated human hepatocellular carcinoma cell lines via modulation of VEGF signaling and PI3K/NF-kappaB p38/caspase-3 axes cross talk. Sorafenib 33-42 caspase 3 Homo sapiens 149-158 35245519-8 2022 The sorafenib-rhamnazin combination also showed significant inhibition of the angiogenicVEGF/VEGFR2/PI3K/NF-kappaBsignaling axis associated with significant upregulation of the apoptotic p38MAPK/caspase-3 axis and inhibition of Ki67, a proliferation marker in HepG2 and HUH-7 cells. Sorafenib 4-13 caspase 3 Homo sapiens 195-204 35245519-9 2022 SIGNIFICANCE: Rhamnazin potentiates the chemotherapeutic effect of sorafenib via modulation ofthe VEGF/PI3K/NF-kappaBsignaling axis, downregulation of VEGFR2 expression, and upregulation of the p38MAPK/caspase-3 axis in human HCC cell lines. Sorafenib 67-76 caspase 3 Homo sapiens 202-211 17909059-4 2007 Sorafenib/TRAIL-induced cell death was accompanied by mitochondrial injury and release of cytochrome c, Smac, and AIF into the cytosol and caspase-9, caspase-3, caspase-7, and caspase-8 activation. Sorafenib 0-9 caspase 3 Homo sapiens 150-159 16985072-3 2006 Sorafenib and bortezomib synergistically induced a marked increase in mitochondrial injury and apoptosis, reflected by cytochrome c release, caspase-3 cleavage, and poly(ADP-ribose) polymerase degradation in a broad range of solid tumor and leukemia cell lines. Sorafenib 0-9 caspase 3 Homo sapiens 141-150 33825398-6 2021 Immunohistochemical analysis of tumor tissues was performed to evaluate the effects of BSJP alone, sorafenib alone, and their combination on the expression of caspase-3, caspase-9, and Bcl-2. Sorafenib 99-108 caspase 3 Homo sapiens 159-168 31389193-7 2019 Finally, it is shown that the combination of sorafenib and AMF induces a higher enzymatic activity of caspase 3 and caspase 9, probably due to an increment in reactive oxygen species by means of hyperthermia. Sorafenib 45-54 caspase 3 Homo sapiens 102-111 31387809-7 2019 Furthermore, sorafenib significantly inhibited cell proliferation, IL-6 level and activation of p-PI3K/AKT while promoted the cell apoptosis rate and Caspase3 level compared as the control group, which were further promoted by administration of si IL-6. Sorafenib 13-22 caspase 3 Homo sapiens 150-158 35234063-9 2022 In the HepG2 xenografts model, sorafenib plus SDC exhibited greater suppression on tumor growth than individual treatment accompanied with decreased expression of VEGF, VEGFA, Ki67, CD31 and increased expression of caspase-3. Sorafenib 31-40 caspase 3 Homo sapiens 215-224 30522045-7 2019 Our results suggest that paclitaxel, sorafenib, and RT synergistically decreased the viability of RCC and breast cancer cells and significantly induced their apoptosis, as shown by caspase-3 cleavage. Sorafenib 37-46 caspase 3 Homo sapiens 181-190 29484394-11 2018 Furthermore, CBI-5725 induced apoptosis more strongly than sorafenib in a dose-dependent manner, which may be attributed to greater caspase-3 and poly(adenosine 5"-diphosphate-ribose) polymerase activation by CBI-5725. Sorafenib 59-68 caspase 3 Homo sapiens 132-141 30030148-5 2018 Synergistic effects of sorafenib and selumetinib on cell apoptosis and phospho-ERK (p-ERK) were analyzed by caspase-3/7 apoptosis assay and western blot, respectively. Sorafenib 23-32 caspase 3 Homo sapiens 108-119 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 caspase 3 Homo sapiens 190-198 26057634-8 2015 Immunohistochemistry analysis of galunisertib and sorafenib-exposed samples showed a significant decrease of the proliferative marker Ki67 and increase of the apoptotic marker caspase-3. Sorafenib 50-59 caspase 3 Homo sapiens 176-185 29072691-11 2017 Finally, PED reduced the antitumoral effect of sorafenib by inhibiting caspase-3/7 activity. Sorafenib 47-56 caspase 3 Homo sapiens 71-80 28096271-0 2017 In Hepatocellular Carcinoma miR-221 Modulates Sorafenib Resistance through Inhibition of Caspase-3-Mediated Apoptosis. Sorafenib 46-55 caspase 3 Homo sapiens 89-98 28142087-9 2017 Our data showed that HNHA and sorafenib synergistically decreased cell viability in ATC cells, and also significantly increased apoptotic cell death in these cells, as proved by the cleavage of caspase-3 and DNA fragmentation. Sorafenib 30-39 caspase 3 Homo sapiens 194-203 27807662-6 2017 Sorafenib plus C2-ceramide stimulated significantly the production of reactive oxygen species (ROS) and mitochondrial depolarization, which promoted caspases-dependent cell apoptosis as illustrated by related protein expression including caspase 3, caspase 9, Bax, Bcl-2, and cytochrome c. Sorafenib 0-9 caspase 3 Homo sapiens 238-247 27863838-0 2016 Resveratrol enhances the efficacy of sorafenib mediated apoptosis in human breast cancer MCF7 cells through ROS, cell cycle inhibition, caspase 3 and PARP cleavage. Sorafenib 37-46 caspase 3 Homo sapiens 136-145 27544320-5 2016 Sorafenib/OA cotreatment induces DNA fragmentation and caspase-3/7 cleavage and the addition of the pan-caspase inhibitor zVAD.fmk shows the requirement of caspase activation for Sorafenib/OA-triggered cell death. Sorafenib 0-9 caspase 3 Homo sapiens 55-64 30132846-6 2018 Small interfering-RNA (si-RNA) assays showed that Bim, but not Bak and Bax, was involved in the induction of caspase-3 in sorafenib-treated HepG2 cells. Sorafenib 122-131 caspase 3 Homo sapiens 109-118 28096271-7 2017 Caspase-3 modulation by miR-221 participates to Sorafenib resistance. Sorafenib 48-57 caspase 3 Homo sapiens 0-9 28110575-8 2017 Sorafenib induced the activation of caspase-3, and its combination with 5-FU more effectively inhibited the growth of xenograft tumors than either sorafenib or 5-FU alone (p < 0.05). Sorafenib 0-9 caspase 3 Homo sapiens 36-45 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 caspase 3 Homo sapiens 191-200 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 caspase 3 Homo sapiens 120-129 26662956-0 2016 Synergistic effect of fisetin combined with sorafenib in human cervical cancer HeLa cells through activation of death receptor-5 mediated caspase-8/caspase-3 and the mitochondria-dependent apoptotic pathway. Sorafenib 44-53 caspase 3 Homo sapiens 148-157 26662956-7 2016 Our study showed that the combination of fisetin and sorafenib exerted better synergistic effects in vitro and in vivo than either agent used alone against human cervical cancer, and this synergism was based on apoptotic potential through a mitochondrial- and DR5-dependent caspase-8/caspase-3 signaling pathway. Sorafenib 53-62 caspase 3 Homo sapiens 284-293 29431086-5 2016 Sorafenib reduces S-nitrosation of cell death receptors and caspase-3, triggering a switch to caspase-3 from caspase-8. Sorafenib 0-9 caspase 3 Homo sapiens 60-69 29431086-5 2016 Sorafenib reduces S-nitrosation of cell death receptors and caspase-3, triggering a switch to caspase-3 from caspase-8. Sorafenib 0-9 caspase 3 Homo sapiens 94-103 26233703-10 2015 In contrast, Sorafenib (10 microM) reduced upstream apoptotic parameters but increased caspase-3 activation and DNA fragmentation in HepG2 cells. Sorafenib 13-22 caspase 3 Homo sapiens 87-96 25136776-4 2014 Treatment of sorafenib still significantly increased caspase-3, bax, cyt-c protein expression and decreased bcl-2 protein in a dose-dependent manner. Sorafenib 13-22 caspase 3 Homo sapiens 53-62 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 caspase 3 Homo sapiens 205-214 25687050-6 2015 Furthermore, sorafenib treatment resulted in the obvious increase of the Caspase-3 and Caspase-8 protein and mRNA expressions, and down-regulated the MCL-1 protein and mRNA expressions in NB4 cells. Sorafenib 13-22 caspase 3 Homo sapiens 73-82 25687050-7 2015 CONCLUSION: Sorafenib can inhibit proliferation and induce apopotosis of human acute promyelocytic leukemia cell NB4 through the expression of Caspase-3 and Caspase-8, and down-regulation of the expression of MCL-1. Sorafenib 12-21 caspase 3 Homo sapiens 143-152 25338583-5 2014 The effects of sorafenib on the expression of caspase-3, BCL-2 and MCL-1 mRNA and protein were assayed by RT-PCR and Western blot respectively. Sorafenib 15-24 caspase 3 Homo sapiens 46-55 25338583-9 2014 Typical apoptotic morphological and ultrastructural changes of MM cells could be observed under transmission electron microscope, Examination of cellular signaling pathways showed that sorafenib induced upregulation of cleaved-caspase-3 expression, and simultaneous downregulation of BCL-2 and MCL-1 expression. Sorafenib 185-194 caspase 3 Homo sapiens 227-236 23497499-11 2013 Sorafenib, alone or in combination with gemcitabine and EMAP, induced apoptosis in HUVECs and WI-38 cells as observed via increased expression of cleaved poly (ADP-ribose) polymerase-1 (PARP-1) and caspase-3 proteins. Sorafenib 0-9 caspase 3 Homo sapiens 198-207 24520095-5 2014 RESULTS: Our data indicate that sorafenib and MPT0E028 synergistically reduced cell viability in liver cancer cells, and also markedly induced apoptotic cell death in these cells, as evidenced by the cleavage of caspase-3, PARP, and DNA fragmentation. Sorafenib 32-41 caspase 3 Homo sapiens 212-221 23732299-7 2013 Prolonged treatment of MDA-MB-231 cells with N"-desmethylsorafenib, N"-desmethylsorafenib N-oxide and sorafenib (10 muM, 72 h) produced small increases in caspase-3 activity to 128-139% of control. Sorafenib 57-66 caspase 3 Homo sapiens 155-164 23243060-4 2013 Sorafenib inhibited platelet-derived growth factor receptor (PDGFR) alpha, TRKA and RON, caused decreases in total and phosphorylated amounts of several signaling molecules, and provoked caspase-3-independent cell death, most likely due to endoplasmic reticulum stress as indicated by upregulation of GADD34 and GADD153 and phosphorylation of PERK. Sorafenib 0-9 caspase 3 Homo sapiens 187-196 22006587-5 2013 Sorafenib along with nutlin-3 synergistically inhibited the cell survival and enhanced caspase-3 cleavage leading to apoptosis in RCC. Sorafenib 0-9 caspase 3 Homo sapiens 87-96