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10.1038/onc.2017.395

http://scihub22266oqcxt.onion/10.1038/onc.2017.395
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C5814337!5814337!29059153
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suck abstract from ncbi


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pmid29059153      Oncogene 2018 ; 37 (7): 924-34
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  • Nutrient sensor O-GlcNAc transferase controls cancer lipid metabolism via SREBP-1 regulation #MMPMID29059153
  • Sodi VL; Bacigalupa ZA; Ferrer CM; Lee JV; Gocal WA; Mukhopadhyay D; Wellen KE; Ivan M; Reginato MJ
  • Oncogene 2018[Feb]; 37 (7): 924-34 PMID29059153show ga
  • Elevated O-GlcNAcylation is associated with disease states such as diabetes and cancer. O-GlcNAc transferase (OGT) is elevated in multiple cancers and inhibition of this enzyme genetically or pharmacologically inhibits oncogenesis. Here we show that O-GlcNAcylation modulates lipid metabolism in cancer cells. OGT regulates expression of the master lipid regulator the transcription factor sterol regulatory element binding protein 1 (SREBP-1) and its transcriptional targets both in cancer and lipogenic tissue. OGT regulates SREBP-1 protein expression via AMP Activated protein kinase (AMPK). SREBP-1 is critical for OGT-mediated regulation of cell survival and of lipid synthesis, as overexpression of SREBP-1 rescues lipogenic defects associated with OGT suppression, and tumor growth in vitro and in vivo. These results unravel a previously unidentified link between O-GlcNAcylation, lipid metabolism and the regulation of SREBP-1 in cancer and suggests a crucial role for O-GlcNAc signaling in transducing nutritional state to regulate lipid metabolism.
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