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10.18632/oncotarget.7935 http://scihub22266oqcxt.onion/10.18632/oncotarget.7935 C4991447!4991447 !26958938     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26958938 &cmd=llinks): Failed to open stream: HTTP request failed! 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Bufalin suppresses hepatocellular carcinoma invasion and metastasis by targeting HIF-1? via the PI3K/AKT/mTOR pathway |pdf=|usr=}}{{26958938 }} gab.com Text Bufalin suppresses hepatocellular carcinoma invasion and metastasis by targeting HIF-1 via the PI3K/AKT/mTOR pathway JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26958938 #FOAvip It has been reported that there are multiple mechanisms by which bufalin could exert its antimetastatic effect. HIF-1? has been reported to be involved in tumor migration and invasion by regulating EMT. However, it is not known whether bufalin could exert the antimetastatic effect by modulating HIF-1? expression in hepatocellular carcinoma. In the present study, we aimed to evaluate the antimetastatic potential of bufalin in vivo and in vitro. Our results demonstrated that the liver/lung metastases were significantly reduced in bufalin-treated mice, as tested in the orthotopic transplanted and tail vein injection tumor models. Furthermore, the epithelial-to-mesenchymal transition (EMT) was inhibited in bufalin-treated tumors, as reflected the upregulation of E-cadherin, and downregulation of N-cadherin, vimentin, Snail. Similar results were observed in SMMC7721 cells treated with bufalin. Moreover, the transforming growth factor-?1 (TGF-?1)-induced EMT was also abrogated by bufalin. Mechanistically, our study demonstrated that hypoxia-inducible factor-1? (HIF-1?) played an important role in the antimetastatic effect of bufalin in hepatocellular carcinoma. Importantly, HIF-1? expression may be regulated through the inhibition of the PI3K/AKT/mTOR pathway. Taken together, our results suggest that bufalin suppresses hepatic tumor invasion and metastasis and that this process may be related to the PI3K/AKT/mTOR/ HIF-1? axis. Twit Text FOAVip Bufalin suppresses hepatocellular carcinoma invasion and metastasis by targeting HIF-1 via the PI3K/AKT/mTOR pathway ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26958938 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26958938 #FOAvip English Wikipedia <ref>{{Cite pmid|26958938 }}</ref> Bufalin suppresses hepatocellular carcinoma invasion and metastasis by targeting HIF-1? via the PI3K/AKT/mTOR pathway #MMPMID26958938 Wang H ; Zhang C ; Xu L ; Zang K ; Ning Z ; Jiang F ; Chi H ; Zhu X ; Meng Z Oncotarget 2016[Apr]; 7 (15 ): 20193-208 PMID26958938 show ga It has been reported that there are multiple mechanisms by which bufalin could exert its antimetastatic effect. HIF-1? has been reported to be involved in tumor migration and invasion by regulating EMT. However, it is not known whether bufalin could exert the antimetastatic effect by modulating HIF-1? expression in hepatocellular carcinoma. In the present study, we aimed to evaluate the antimetastatic potential of bufalin in vivo and in vitro. Our results demonstrated that the liver/lung metastases were significantly reduced in bufalin-treated mice, as tested in the orthotopic transplanted and tail vein injection tumor models. Furthermore, the epithelial-to-mesenchymal transition (EMT) was inhibited in bufalin-treated tumors, as reflected the upregulation of E-cadherin, and downregulation of N-cadherin, vimentin, Snail. Similar results were observed in SMMC7721 cells treated with bufalin. Moreover, the transforming growth factor-?1 (TGF-?1)-induced EMT was also abrogated by bufalin. Mechanistically, our study demonstrated that hypoxia-inducible factor-1? (HIF-1?) played an important role in the antimetastatic effect of bufalin in hepatocellular carcinoma. Importantly, HIF-1? expression may be regulated through the inhibition of the PI3K/AKT/mTOR pathway. Taken together, our results suggest that bufalin suppresses hepatic tumor invasion and metastasis and that this process may be related to the PI3K/AKT/mTOR/ HIF-1? axis. |*Phosphoinositide-3 Kinase Inhibitors [MESH] |Animals [MESH] |Antineoplastic Agents/pharmacology [MESH] |Apoptosis [MESH] |Biomarkers, Tumor/metabolism [MESH] |Bufanolides/*pharmacology [MESH] |Carcinoma, Hepatocellular/*drug therapy/metabolism/secondary [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Epithelial-Mesenchymal Transition [MESH] |Gene Expression Regulation, Neoplastic/drug effects [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*antagonists & inhibitors/metabolism [MESH] |Liver Neoplasms/*drug therapy/metabolism/pathology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Nude [MESH] |Neoplasm Invasiveness [MESH] |Neoplasm Metastasis [MESH] |Phosphatidylinositol 3-Kinases/metabolism [MESH] |Proto-Oncogene Proteins c-akt/*antagonists & inhibitors/metabolism [MESH] |Signal Transduction [MESH] |TOR Serine-Threonine Kinases/*antagonists & inhibitors/metabolism [MESH] |Transforming Growth Factor beta1/metabolism [MESH] |Tumor Cells, Cultured [MESH]Bufalin suppresses hepatocellular carcinoma invasion and metastasis by(epmc).pdf DeepDyve Pubget Overpricing