Oncotarget

Research Papers:

Yin Yang-1 increases apoptosis through Bax activation in pancreatic cancer cells

Jing-Jing Zhang _, Yi Zhu, Chuang Yang, Xian Liu, Yun-Peng Peng, Kui-Rong Jiang, Yi Miao and Ze-Kuan Xu

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Oncotarget. 2016; 7:28498-28509. https://doi.org/10.18632/oncotarget.8654

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Abstract

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.


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