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On-line Access: 2018-06-04

Received: 2017-03-15

Revision Accepted: 2017-06-12

Crosschecked: 2018-05-14

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Qing-hua Cui


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Journal of Zhejiang University SCIENCE B 2018 Vol.19 No.6 P.415-424


PGC-1α coordinates with Bcl-2 to control the cell cycle in U251 cells through reducing ROS

Author(s):  Kun Yao, Xu-feng Fu, Xing Du, Yan Li, Shan-shan Yang, Min Yu, Qing-hua Cui

Affiliation(s):  School of Life Sciences, Yunnan University, Kunming 650091, China; more

Corresponding email(s):   cuiqinghua@ynu.edu.cn

Key Words:  B-cell lymphoma 2 (Bcl-2), Peroxisome proliferator-activated receptor-γ, co-activator 1α, (PGC-1α, ), Mitochondria, Reactive oxygen species (ROS), Cell cycle

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Kun Yao, Xu-feng Fu, Xing Du, Yan Li, Shan-shan Yang, Min Yu, Qing-hua Cui. PGC-1α coordinates with Bcl-2 to control the cell cycle in U251 cells through reducing ROS[J]. Journal of Zhejiang University Science B, 2018, 19(6): 415-424.

@article{title="PGC-1α coordinates with Bcl-2 to control the cell cycle in U251 cells through reducing ROS",
author="Kun Yao, Xu-feng Fu, Xing Du, Yan Li, Shan-shan Yang, Min Yu, Qing-hua Cui",
journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T PGC-1α coordinates with Bcl-2 to control the cell cycle in U251 cells through reducing ROS
%A Kun Yao
%A Xu-feng Fu
%A Xing Du
%A Yan Li
%A Shan-shan Yang
%A Min Yu
%A Qing-hua Cui
%J Journal of Zhejiang University SCIENCE B
%V 19
%N 6
%P 415-424
%@ 1673-1581
%D 2018
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1700148

T1 - PGC-1α coordinates with Bcl-2 to control the cell cycle in U251 cells through reducing ROS
A1 - Kun Yao
A1 - Xu-feng Fu
A1 - Xing Du
A1 - Yan Li
A1 - Shan-shan Yang
A1 - Min Yu
A1 - Qing-hua Cui
J0 - Journal of Zhejiang University Science B
VL - 19
IS - 6
SP - 415
EP - 424
%@ 1673-1581
Y1 - 2018
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1700148

B-cell lymphoma 2 (Bcl-2) has a dual function, acting as both an oncogene and an anti-tumor gene. It is well known that Bcl-2 exerts its tumor promoting function through the mitochondrial pathway. However, the mechanism by which it suppresses tumor formation is not well understood. We have previously shown that Bcl-2 inhibits cell cycle progression from the G0/G1 to the S phase after serum starvation, and that quiescent Bcl-2 expressing cells maintain a significantly lower level of mitochondrial reactive oxygen species (ROS) than control cells. Based on the fact that ROS mediate cell cycle progression and are controlled by peroxisome proliferator-activated receptor-γ; co-activator 1α; (PGC-1α;), a key molecule induced by prolonged starvation and involved in mitochondrial metabolism, we hypothesized that PGC-1α might be related to the cell cycle function of Bcl-2. In this paper, we show that PGC-1α is upregulated by Bcl-2 overexpression and downregulated following Bcl-2 knockdown or downregulation after serum starvation. However, Bcl-2 is negatively regulated by PGC-1α expression. Further, co-immunoprecipitation (co-IP) experiments showed that PGC-1α protein is co-precipitated with Bcl-2 at the G0/G1 phase. Taken together, our results suggest that PGC-1α interacts with Bcl-2 after serum depletion, and that Bcl-2 might recruit PGC-1α to reduce ROS, which in turn delays cell cycle progression in coordination with Bcl-2.


目的:探究过氧化物酶体增生激活受体γ协同刺激因子1α (PGC-1α)和B细胞淋巴瘤-2(Bcl-2)在调控细胞周期中的相互关系.
方法:用蛋白质印迹法(Western blotting)检测了接触抑制和血清饥饿处理的NIH3T3过表达Bcl-2的细胞中PGC-1α的表达,并且分别检测了用Bcl-2和PGC-1α的小干扰RNA(siRNA)降低U251细胞(内源性高表达Bcl-2和PGC-1α)中的Bcl-2和PGC-1α的表达,最后用免疫共沉淀(co-IP)检测了二者的关系.

关键词:过氧化物酶体增生激活受体γ协同刺激因子1α (PGC-1α);B细胞淋巴瘤-2(Bcl-2);线粒体;活性氧自由基(ROS);细胞周期

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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[28]List of electronic supplementary materials

[29]Fig. S1 Immunofluorescence images of PGC-1α and Bcl-2 protein co-localization in NIH3T3 cells

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