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10.1186/s13046-018-0808-1 http://scihub22266oqcxt.onion/10.1186/s13046-018-0808-1 C6042396!6042396 !29996891     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29996891 &cmd=llinks): Failed to open stream: HTTP request failed! 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STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer |pdf=|usr=}}{{29996891 }} gab.com Text STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer JO: J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=29996891 #FOAvip BACKGROUND: Serine/threonine protein kinase 25 (STK25) is critical in regulating whole-body glucose and insulin homeostasis and the accumulation of ectopic lipids. The Warburg effect, also known as aerobic glycolysis, is an essential metabolic characteristic of cancer cells. However, the effects of STK25 on aerobic glycolysis of cancer cells remain unexplored. The aim of this study is to investigate the role of STK25 in colorectal cancer (CRC) and to elucidate the underlying mechanisms. METHODS: The influences of STK25 on the cell proliferation were evaluated by MTT and colony formation assays. The roles of STK25 in aerobic glycolysis were determined by glucose uptake and lactate production assays. The interaction between STK25 and GOLPH3 was detected by co-immunoprecipitation, GST pull-down, and His-tag pull-down assays. Western blot was used to measure the expression of glycolytic genes, and the status of kinases in mTOR pathway. Moreover, a xenograft mouse model was used to investigate the effects of STK25 in vivo. The prognostic significance of STK25 was analyzed using public CRC datasets by a log-rank test. RESULTS: STK25 suppressed proliferation, glycolysis and glycolytic gene expression in CRC cells. STK25 interacted with GOLPH3 and mediated glycolysis through GOLPH3-regulated mTOR signaling. Consistent with these observations, silencing of STK25 promoted tumor growth and glycolytic gene expression in an in vivo xenograft mouse model. Moreover, high levels of STK25 correlated with favorable prognosis in patients with CRC. CONCLUSIONS: Our results demonstrated that STK25 negatively regulates the proliferation and glycolysis via GOLPH3-dependent mTOR signaling. Accordingly, STK25 could be a potential therapeutic target for the treatment of CRC. Twit Text FOAVip STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer ????J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=29996891 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29996891 #FOAvip English Wikipedia <ref>{{Cite pmid|29996891 }}</ref> STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer #MMPMID29996891 Wu F ; Gao P ; Wu W ; Wang Z ; Yang J ; Di J ; Jiang B ; Su X J Exp Clin Cancer Res 2018[Jul]; 37 (1 ): 144 PMID29996891 show ga BACKGROUND: Serine/threonine protein kinase 25 (STK25) is critical in regulating whole-body glucose and insulin homeostasis and the accumulation of ectopic lipids. The Warburg effect, also known as aerobic glycolysis, is an essential metabolic characteristic of cancer cells. However, the effects of STK25 on aerobic glycolysis of cancer cells remain unexplored. The aim of this study is to investigate the role of STK25 in colorectal cancer (CRC) and to elucidate the underlying mechanisms. METHODS: The influences of STK25 on the cell proliferation were evaluated by MTT and colony formation assays. The roles of STK25 in aerobic glycolysis were determined by glucose uptake and lactate production assays. The interaction between STK25 and GOLPH3 was detected by co-immunoprecipitation, GST pull-down, and His-tag pull-down assays. Western blot was used to measure the expression of glycolytic genes, and the status of kinases in mTOR pathway. Moreover, a xenograft mouse model was used to investigate the effects of STK25 in vivo. The prognostic significance of STK25 was analyzed using public CRC datasets by a log-rank test. RESULTS: STK25 suppressed proliferation, glycolysis and glycolytic gene expression in CRC cells. STK25 interacted with GOLPH3 and mediated glycolysis through GOLPH3-regulated mTOR signaling. Consistent with these observations, silencing of STK25 promoted tumor growth and glycolytic gene expression in an in vivo xenograft mouse model. Moreover, high levels of STK25 correlated with favorable prognosis in patients with CRC. CONCLUSIONS: Our results demonstrated that STK25 negatively regulates the proliferation and glycolysis via GOLPH3-dependent mTOR signaling. Accordingly, STK25 could be a potential therapeutic target for the treatment of CRC. |*Signal Transduction [MESH] |Animals [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation [MESH] |Colorectal Neoplasms/diagnostic imaging/genetics/*metabolism [MESH] |Disease Models, Animal [MESH] |Gene Expression Profiling [MESH] |Glucose/metabolism [MESH] |Glycolysis/drug effects [MESH] |Humans [MESH] |Intracellular Signaling Peptides and Proteins/genetics/*metabolism [MESH] |Lactic Acid/biosynthesis [MESH] |Membrane Proteins/*metabolism [MESH] |Mice [MESH] |Prognosis [MESH] |Protein Serine-Threonine Kinases/genetics/*metabolism [MESH] |TOR Serine-Threonine Kinases/*metabolism [MESH]STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway(epmc).pdf DeepDyve Pubget Overpricing