Open AccessYin Yang-1 increases apoptosis through Bax activation in pancreatic cancer cells
Author(s) -
Jingjing Zhang,
Yaping Zhu,
Chuang Yang,
Xian Liu,
Yunpeng Peng,
Kuirong Jiang,
Yi Miao,
Zekuan Xu
Publication year - 2016
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.8654
Subject(s) - apoptosis , pancreatic cancer , chromatin immunoprecipitation , cancer research , medicine , yy1 , cancer , microbiology and biotechnology , biology , promoter , gene expression , gene , genetics
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.