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

By Kun Yao, Xufeng Fu, Du Xing, Yan Li, Bing Han, Chen Zexi, Shanshan Yang, Ran Wei, Jiaqi Zhou, Qinghua Cui

Posted 24 Feb 2017
bioRxiv DOI: 10.1101/111567 (published DOI: 10.1631/jzus.B1700148)

B-cell lymphoma 2 (Bcl-2) has a dual function, acting both as 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 Bcl-2 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 maintained a significant lower level of mitochondrial reactive oxygen species (ROS) than the 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 with the cell cycle function of Bcl-2. Here, we showed that PGC-1α was upregulated upon Bcl-2 overexpression and downregulated following Bcl-2 knockdown during serum starvation. Knockdown of PGC-1α activated Bcl-2 expression. Taken together, our results suggest that after serum depletion, PGC-1α might coordinate with Bcl-2 to reduce ROS, which in turn delay cell cycle progression.

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