Research Papers:
Yin Yang1 increases apoptosis through Bax activation in pancreatic cancer cells
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Jing-Jing Zhang1,2,3,*, Yi Zhu1,2,3,*, Chuang Yang1,2,3, Xian Liu1,2,3, Yun-Peng Peng1,2,3, Kui-Rong Jiang1,2,3, Yi Miao1,2,3, Ze-Kuan Xu3
1Pancreas Institute of Nanjing Medical University, Nanjing 210029, People’s Republic of China
2Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, People’s Republic of China
3Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, People’s Republic of China
*These authors contributed equally to this work
Correspondence to:
Yi Miao, email: [email protected]
Ze-kuan Xu, email: [email protected]
Keywords: Yin Yang-1, pancreatic cancer, apoptosis, Bax
Received: January 28, 2016 Accepted: March 28, 2016 Published: April 08, 2016
ABSTRACT
The transcriptional regulator Yin Yang-1 (YY1) is a tumor suppressor known to be overexpressed in pancreatic cancer. We found that overexpression of YY1 promoted apoptosis and increased the expression and mitochondrial localization of the pro-apoptotic Bax protein in pancreatic cancer cell lines. Luciferase reporter, electrophoretic mobility shift (EMSA), and chromatin immunoprecipitation (ChIP) assays revealed binding of YY1 to the BAX promoter. Moreover, YY1 promoted pancreatic cancer cell apoptosis through Bax transcriptional activation and subsequent translocation of Bax to the mitochondrial membrane, leading to cytochrome c release, and caspase activation.YY1 and BAX are co-expressed in pancreatic cancer tissues and higher BAX expression predicts better outcomes for patients. The ability of YY1 to promote apoptosis in pancreatic cancer cells suggests it may represent a valuable diagnostic and therapeutic target.