Title : AMPK-deficiency forces metformin-challenged cancer cells to switch from carbohydrate metabolism to ketogenesis to support energy metabolism.

Pub. Date : 2021 Sep

PMID : 34290400






5 Functional Relationships(s)
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1 To date most of the anti-cancer properties of metformin have, in large part, been attributed either to the inhibition of mitochondrial NADH oxidase complex (Complex I in the electron transport chain) or the activation of AMP-activated kinase (AMPK). Metformin protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens
2 To date most of the anti-cancer properties of metformin have, in large part, been attributed either to the inhibition of mitochondrial NADH oxidase complex (Complex I in the electron transport chain) or the activation of AMP-activated kinase (AMPK). Metformin protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens
3 However, it is becoming increasingly clear that AMPK activation may be critical to alleviate metabolic and energetic stresses associated with tumor progression suggesting that it may, in fact, attenuate the toxicity of metformin instead of promoting it. Metformin protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens
4 We also found that metformin forces cells to rewire their metabolic grid in a manner that depends on AMPK, with AMPK-competent cells upregulating glycolysis and AMPK-deficient cell resorting to ketogenesis. Metformin protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens
5 We also found that metformin forces cells to rewire their metabolic grid in a manner that depends on AMPK, with AMPK-competent cells upregulating glycolysis and AMPK-deficient cell resorting to ketogenesis. Metformin protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens