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. 2017 Dec 27;12(12):e0190241. doi: 10.1371/journal.pone.0190241

Fig 13. The Acss2/Cbp/Sirt1/HIF-2 axis regulates tumor cell growth and metastasis.

Fig 13

An acetate switch controls Cbp/HIF-2α interactions during stress, which is activated by increased endogenous acetate generated in response to stress. Oral acetate also activates the acetate switch to stimulate tumor cell function, which potentially links tumor growth and metastasis with nutritional cues. Nuclear-localized Acss2 is the molecular mediator of the acetate switch and supplies Cbp with a specific pool of nuclear acetyl CoA used in the acetylation of HIF-2α. Cbp and HIF-2α act in concert as a downstream effector of the acetate switch to regulate genetic as well as epigenetic events. Sirt1 regenerates deacetylated HIF-2α, which undergoes repetitive acetylation as long as the nuclear acetyl CoA pool from Acss2 is present.