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SENP3 Postpones Cellular Senescence of P53-mediated Pathway under Mild Oxidative Stress


Zu-Jun Sun, Jing Yi, Yu-Mei Wang*
Department of Cell Biology, Key Laboratory of the Education Ministry for Cell Differentiation and Apoptosis, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
Abstract: The p53 tumor suppressor functions as a transcription factor which becomes activated upon a number of diverse stress stimuli including DNA damage, oncogene overexpression or metabolic limitations. Upon activation, p53 triggers growth arrest or apoptosis, which serves to eliminate heavily damaged cells. In 50% of human cancers, the gene encoding p53 is mutated. In the remaining cancers, however, p53 retains its wild-type status but its function is effectively inhibited, little is known the reason. We found that SENP3 protein level was enhanced under mild oxidative stress. Meanwhile, SENP3 dispersed from nucleolus to nuclearplasm. The transcriptional activity of p53 was repressed by overexpression of SENP3. The results showed that overexpression of SENP3 could result in inactivation of p53, and may postpone cell senescence in response to mild oxidative stress. This research will provide a new clew for explaining of p53 inactivation.


CSTR: 32200.14.cjcb.2009.03.0014