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10.1016/j.cmet.2016.03.008

http://scihub22266oqcxt.onion/10.1016/j.cmet.2016.03.008
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suck abstract from ncbi


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pmid27076078
      Cell+Metab 2016 ; 23 (4 ): 649-62
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  • AMPK Is Essential to Balance Glycolysis and Mitochondrial Metabolism to Control T-ALL Cell Stress and Survival #MMPMID27076078
  • Kishton RJ ; Barnes CE ; Nichols AG ; Cohen S ; Gerriets VA ; Siska PJ ; Macintyre AN ; Goraksha-Hicks P ; de Cubas AA ; Liu T ; Warmoes MO ; Abel ED ; Yeoh AE ; Gershon TR ; Rathmell WK ; Richards KL ; Locasale JW ; Rathmell JC
  • Cell Metab 2016[Apr]; 23 (4 ): 649-62 PMID27076078 show ga
  • T cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy associated with Notch pathway mutations. While both normal activated and leukemic T cells can utilize aerobic glycolysis to support proliferation, it is unclear to what extent these cell populations are metabolically similar and if differences reveal T-ALL vulnerabilities. Here we show that aerobic glycolysis is surprisingly less active in T-ALL cells than proliferating normal T cells and that T-ALL cells are metabolically distinct. Oncogenic Notch promoted glycolysis but also induced metabolic stress that activated 5' AMP-activated kinase (AMPK). Unlike stimulated T cells, AMPK actively restrained aerobic glycolysis in T-ALL cells through inhibition of mTORC1 while promoting oxidative metabolism and mitochondrial Complex I activity. Importantly, AMPK deficiency or inhibition of Complex I led to T-ALL cell death and reduced disease burden. Thus, AMPK simultaneously inhibits anabolic growth signaling and is essential to promote mitochondrial pathways that mitigate metabolic stress and apoptosis in T-ALL.
  • |*Glycolysis [MESH]
  • |AMP-Activated Protein Kinases/*metabolism [MESH]
  • |Animals [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Survival [MESH]
  • |Humans [MESH]
  • |Mechanistic Target of Rapamycin Complex 1 [MESH]
  • |Mice, Inbred C57BL [MESH]
  • |Mitochondria/*metabolism/pathology [MESH]
  • |Multiprotein Complexes/metabolism [MESH]
  • |Precursor Cell Lymphoblastic Leukemia-Lymphoma/*metabolism/pathology [MESH]
  • |Receptors, Notch/metabolism [MESH]
  • |Signal Transduction [MESH]
  • |Stress, Physiological [MESH]
  • |T-Lymphocytes/metabolism/pathology [MESH]


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