Is it a potential cancer therapy by preventing acetate capture?
Is it a potential cancer therapy by preventing acetate capture?
 Acetyl-CoA is a metabolic intermediate converted from acetate and it has recently been shown to promote lipid synthesis and tumor growth. Its conversion enzyme ACSS2 (Acetyl-CoA synthetase 2) was upregulated in various cancer cells and loss of ACSS2 decreased tumor growth. However, the molecular mechanism how acetate and ACSS enhance tumor growth is unclear. A recent article published on Nature Communications by Dr. Gao and his colleagues shows that acetate mediates epigenetic regulation and promotes tumor growth under hypoxic stress. It’s shown that acetate enhances acetylation of histone H3 which activates lipogenic genes ACACA and FASN expression, thus promoting lipid synthesis and cell survival in an ACSS1/2-dependent manner. Acetyl-CoA synthetases positively regulate histone H3 acetylation and the following FASN expression. This study demonstrates that acetate not only induces fatty acid synthesis as a metabolic precursor, but also acts as an epigenetic metabolite to promote cancer cell survival. Fight cancer with arigo’s superior antibodies for the study of epigenesis and lipid metabolism!
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| ChIP assay by Histone H3 acetyl (Lys9) antibody (ARG54755) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Reference:
Gao et al. (2016) Nat Commun. 7:11960.
