抑制 SIRT2 和改变人类多能干细胞的乙酰化状态：在重编程过程中代谢转换的可能联系。

Suppression of SIRT2 and altered acetylation status of human pluripotent stem cells: possible link to metabolic switch during reprogramming.

机构信息

College of Natural Sciences, Department of Life Sciences, Sogang University, Seoul 04107, Korea.

Department of Hematology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.

出版信息

BMB Rep. 2017 Sep;50(9):435-436. doi: 10.5483/bmbrep.2017.50.9.119.

DOI:10.5483/bmbrep.2017.50.9.119

PMID:28683850

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5625689/

Abstract

Primed human pluripotent stem cells (hPSCs) are highly dependent on glycolysis rather than oxidative phosphorylation, which is similar to the metabolic switch that occurs in cancer cells. However, the molecular mechanisms that underlie this metabolic reprogramming in hPSCs and its relevance to pluripotency remain unclear. Cha et al. (2017) recently revealed that downregulation of SIRT2 by miR-200c enhances acetylation of glycolytic enzymes and glycolysis, which in turn facilitates cellular reprogramming, suggesting that SIRT2 is a key enzyme linking the metabolic switch and pluripotency in hPSCs. [BMB Reports 2017; 50(9): 435-436].

摘要

人多能干细胞（hPSCs）在经过诱导后，其代谢途径高度依赖糖酵解，而非氧化磷酸化，这与癌细胞中的代谢转换非常相似。然而，hPSCs 中这种代谢重编程的分子机制及其与多能性的相关性仍不清楚。Cha 等人。（2017 年）最近揭示了 miR-200c 下调 SIRT2 可增强糖酵解酶和糖酵解的乙酰化，这反过来又促进了细胞重编程，表明 SIRT2 是连接 hPSCs 代谢转换和多能性的关键酶。[BMB 报告 2017；50（9）：435-436]。