期刊
EXPERIMENTAL CELL RESEARCH
卷 315, 期 16, 页码 2765-2774出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2009.06.024
关键词
Apoptosis; Caloric restriction; PKM2; Proliferation; Growth; Metabolic activity
资金
- Austrian Cancer Society-Tyrol
The glycolytic key regulator pyruvate kinase M2 (M2-PK or PKM2) call switch between a highly active tetrameric and all inactive dimeric form. The transition between the two conformations regulates the glycolytic flux in tumor cells. We developed specific M2-PK-binding peptide aptamers which inhibit M2-PK, but not the 96% homologous M1-PK isoenzyme. In this Study we demonstrate that, at normal blood glucose concentrations, peptide aptamer-mediated inhibition of M2-PK induces a significant decrease of the population doubling (PDL rate) and cell proliferation rate as well as all increase in cell size, whereas Under glucose restriction in increase in PDL and cell proliferation rates but a decrease in cell size was observed. Moreover, M2-PK inhibition rescues cells from glucose starvation-induced apoptotic cell death by increasing the metabolic activity. These findings Suggest that M2-PK is a metabolic sensor which regulates Cell proliferation, cell growth and apoptotic cell death in a glucose supply-dependent manner. (C) 2009 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据