PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29207653-0 2017 Melatonin enhances sorafenib actions in human hepatocarcinoma cells by inhibiting mTORC1/p70S6K/HIF-1alpha and hypoxia-mediated mitophagy. Sorafenib 19-28 CREB regulated transcription coactivator 1 Mus musculus 82-88 28687354-0 2017 Aspirin disrupts the mTOR-Raptor complex and potentiates the anti-cancer activities of sorafenib via mTORC1 inhibition. Sorafenib 87-96 CREB regulated transcription coactivator 1 Mus musculus 101-107 28687354-7 2017 Additionally, the combination of aspirin and sorafenib showed synergetic effects via inhibiting mTORC1 signaling and the PI3K/AKT, MAPK/ERK pathways. Sorafenib 45-54 CREB regulated transcription coactivator 1 Mus musculus 96-102 29251327-8 2018 Simultaneous administration of everolimus to suppress activated mTORC1 in RBE cells revealed that combined everolimus and sorafenib treatment under mTORC2 disassembly could enhance growth inhibition through the suppression of both sorafenib- and everolimus-dependent AKT Ser473 phosphorylation in addition to the inhibition of mTORC1 phosphorylation. Sorafenib 122-131 CREB regulated transcription coactivator 1 Mus musculus 64-70 29251327-8 2018 Simultaneous administration of everolimus to suppress activated mTORC1 in RBE cells revealed that combined everolimus and sorafenib treatment under mTORC2 disassembly could enhance growth inhibition through the suppression of both sorafenib- and everolimus-dependent AKT Ser473 phosphorylation in addition to the inhibition of mTORC1 phosphorylation. Sorafenib 122-131 CREB regulated transcription coactivator 1 Mus musculus 327-333 29251327-8 2018 Simultaneous administration of everolimus to suppress activated mTORC1 in RBE cells revealed that combined everolimus and sorafenib treatment under mTORC2 disassembly could enhance growth inhibition through the suppression of both sorafenib- and everolimus-dependent AKT Ser473 phosphorylation in addition to the inhibition of mTORC1 phosphorylation. Sorafenib 231-240 CREB regulated transcription coactivator 1 Mus musculus 64-70 27959383-4 2017 Sorafenib effectively reversed the activation status of mTORC2 induced by metformin and enhanced the suppression of the mTORC1 and MAPK pathway by metformin in HCC cells, which may be responsible for reduced proliferation upon combined treatment. Sorafenib 0-9 CREB regulated transcription coactivator 1 Mus musculus 120-126 28276433-5 2017 However, over the past decade, marked advances in the treatment of metastatic RCC have been made, with targeted agents including sorafenib, sunitinib, bevacizumab, pazopanib and axitinib, which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGFR), and everolimus and temsirolimus, which inhibit mechanistic target of rapamycin complex 1 (mTORC1), being approved. Sorafenib 129-138 CREB regulated transcription coactivator 1 Mus musculus 360-366 27959383-5 2017 The metformin and sorafenib combination led to increased impaired proliferation and tumor inhibition of HCC in vitro and in vivo compared to single agent, which was partially bridged by disrupting the mTORC1/mTORC2 feedback loop. Sorafenib 18-27 CREB regulated transcription coactivator 1 Mus musculus 201-207 23963659-9 2013 This previously unrecognized long-term effect of sorafenib was mediated by AMPK-dependent inhibition of the mTORC1 pathway. Sorafenib 49-58 CREB regulated transcription coactivator 1 Mus musculus 108-114 23963659-10 2013 Suppression of mTORC1 activity was sufficient for sorafenib to hinder glucose utilization in breast cancer cells, as demonstrated by the observation that the mTORC1 inhibitor rapamycin induced a comparable down-regulation of GLUT-1 expression and glucose uptake. Sorafenib 50-59 CREB regulated transcription coactivator 1 Mus musculus 15-21 23963659-10 2013 Suppression of mTORC1 activity was sufficient for sorafenib to hinder glucose utilization in breast cancer cells, as demonstrated by the observation that the mTORC1 inhibitor rapamycin induced a comparable down-regulation of GLUT-1 expression and glucose uptake. Sorafenib 50-59 CREB regulated transcription coactivator 1 Mus musculus 158-164 23963659-11 2013 The key role of AMPK-dependent inhibition of mTORC1 in sorafenib mechanisms of action was confirmed by AMPKalpha1 silencing, which restored mTORC1 activity conferring a significant protection from cell death. Sorafenib 55-64 CREB regulated transcription coactivator 1 Mus musculus 45-51 23963659-11 2013 The key role of AMPK-dependent inhibition of mTORC1 in sorafenib mechanisms of action was confirmed by AMPKalpha1 silencing, which restored mTORC1 activity conferring a significant protection from cell death. Sorafenib 55-64 CREB regulated transcription coactivator 1 Mus musculus 140-146 23434734-0 2013 The Combination of Sorafenib and Everolimus Abrogates mTORC1 and mTORC2 upregulation in osteosarcoma preclinical models. Sorafenib 19-28 CREB regulated transcription coactivator 1 Mus musculus 54-60 23434734-9 2013 RESULTS: After sorafenib treatment, mTORC1 signaling was reduced (downstream target P-S6), whereas mTORC2 was increased (phospho-mTOR Ser2481) in MNNG-HOS xenografts compared with vehicle-treated mice. Sorafenib 15-24 CREB regulated transcription coactivator 1 Mus musculus 36-42 23434734-10 2013 Combining sorafenib with everolimus resulted in complete abrogation of both mTORC1 [through ROS-mediated AMP-activated kinase (AMPK) activation] and mTORC2 (through complex disassembly). Sorafenib 10-19 CREB regulated transcription coactivator 1 Mus musculus 76-82 35234063-0 2022 Combination of ShuangDan Capsule and Sorafenib Inhibits Tumor Growth and Angiogenesis in Hepatocellular Carcinoma Via PI3K/Akt/mTORC1 Pathway. Sorafenib 37-46 CREB regulated transcription coactivator 1 Mus musculus 127-133 20054642-4 2010 Sorafenib inhibited cell proliferation in a concentration-dependent manner; this effect was not dependent on sorafenib-mediated inhibition of Raf1, but involved the down-regulation of mTORC1 and its targets p70S6K and 4E-binding protein 1 (4E-BP1). Sorafenib 0-9 CREB regulated transcription coactivator 1 Mus musculus 184-190 34247189-9 2021 The synergy between Terbinafine and sorafenib was due to concomitant inhibition of mTORC1 and induction of severe persistent DNA double-strand breaks (DSBs), which led to the delayed proliferation and accelerated cell death. Sorafenib 36-45 CREB regulated transcription coactivator 1 Mus musculus 83-89