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10.1111/jcmm.13202 http://scihub22266oqcxt.onion/10.1111/jcmm.13202 C5661146!5661146 !28544376     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28544376 &cmd=llinks): Failed to open stream: HTTP request failed! 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HIF-2? regulates non-canonical glutamine metabolism via activation of PI3K/mTORC2 pathway in human pancreatic ductal adenocarcinoma |pdf=|usr=}}{{28544376 }} gab.com Text HIF-2 regulates non-canonical glutamine metabolism via activation of PI3K/mTORC2 pathway in human pancreatic ductal adenocarcinoma JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28544376 #FOAvip Hypoxia-inducible factor-2? (HIF-2?) plays an important role in increasing cancer progression and distant metastasis in a variety of tumour types. We aimed to investigate its biological function and clinical significance in human pancreatic ductal adenocarcinoma (PDAC). A total of 283 paired PDAC tissues and adjacent normal tissues were collected from patients who underwent surgery or biopsy at Sun Yat-sen Memorial Hospital between February 2004 and October 2016. In this study, we noted that HIF-2? expression was significantly up-regulated in PDAC, positively associated with disease stage, lymph-node metastasis and patient survival, and identified as an independent prognostic factor of PDAC patients. We demonstrated that HIF-2? silencing could reduce proliferation, migration and invasion of PDAC cells in vitro. The similar effect on growth was demonstrated in vivo. Furthermore, we noted that knock-down of HIF-2? significantly decreased the expression of glutamate oxaloacetate transaminase 1 (GOT1). Importantly, we confirmed that the PI3K/mTORC2 pathway promoted GOT1 expression by targeting HIF-2?. Our study validated HIF-2? was an important factor in PDAC progression and poor prognosis and may promote non-canonical glutamine metabolism via activation of PI3K/mTORC2 pathway. Targeting HIF-2? represents a novel prognostic biomarker and therapeutic target for patients with PDAC. Twit Text FOAVip HIF-2 regulates non-canonical glutamine metabolism via activation of PI3K/mTORC2 pathway in human pancreatic ductal adenocarcinoma ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28544376 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28544376 #FOAvip English Wikipedia <ref>{{Cite pmid|28544376 }}</ref> HIF-2? regulates non-canonical glutamine metabolism via activation of PI3K/mTORC2 pathway in human pancreatic ductal adenocarcinoma #MMPMID28544376 Li W ; Chen C ; Zhao X ; Ye H ; Zhao Y ; Fu Z ; Pan W ; Zheng S ; Wei L ; Nong T ; Li Z ; Chen R J Cell Mol Med 2017[Nov]; 21 (11 ): 2896-2908 PMID28544376 show ga Hypoxia-inducible factor-2? (HIF-2?) plays an important role in increasing cancer progression and distant metastasis in a variety of tumour types. We aimed to investigate its biological function and clinical significance in human pancreatic ductal adenocarcinoma (PDAC). A total of 283 paired PDAC tissues and adjacent normal tissues were collected from patients who underwent surgery or biopsy at Sun Yat-sen Memorial Hospital between February 2004 and October 2016. In this study, we noted that HIF-2? expression was significantly up-regulated in PDAC, positively associated with disease stage, lymph-node metastasis and patient survival, and identified as an independent prognostic factor of PDAC patients. We demonstrated that HIF-2? silencing could reduce proliferation, migration and invasion of PDAC cells in vitro. The similar effect on growth was demonstrated in vivo. Furthermore, we noted that knock-down of HIF-2? significantly decreased the expression of glutamate oxaloacetate transaminase 1 (GOT1). Importantly, we confirmed that the PI3K/mTORC2 pathway promoted GOT1 expression by targeting HIF-2?. Our study validated HIF-2? was an important factor in PDAC progression and poor prognosis and may promote non-canonical glutamine metabolism via activation of PI3K/mTORC2 pathway. Targeting HIF-2? represents a novel prognostic biomarker and therapeutic target for patients with PDAC. |*Gene Expression Regulation, Neoplastic [MESH] |Aged [MESH] |Animals [MESH] |Aspartate Aminotransferase, Cytoplasmic/genetics/*metabolism [MESH] |Basic Helix-Loop-Helix Transcription Factors/antagonists & inhibitors/genetics/*metabolism [MESH] |Carcinoma, Pancreatic Ductal/genetics/*metabolism/mortality/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Female [MESH] |Glutamine/metabolism [MESH] |Humans [MESH] |Lymphatic Metastasis [MESH] |Male [MESH] |Mechanistic Target of Rapamycin Complex 2/genetics/*metabolism [MESH] |Mice, Nude [MESH] |Middle Aged [MESH] |Neoplasm Staging [MESH] |Neoplasm Transplantation [MESH] |Pancreatic Neoplasms/genetics/*metabolism/mortality/pathology [MESH] |Phosphatidylinositol 3-Kinases/genetics/*metabolism [MESH] |RNA, Small Interfering/genetics/metabolism [MESH] |Signal Transduction [MESH]HIF-2? regulates non-canonical glutamine metabolism via activation of (epmc).pdf DeepDyve Pubget Overpricing