EBP50 regulates the apoptosis of pancreatic cancer cells by decreasing the expression levels of Bcl-2
Author(s) -
Mengyao Ji,
Lei Yuan,
LV Xiao-guang,
Weiguo Dong,
Xiulan Peng
Publication year - 2014
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2014.1831
Subject(s) - apoptosis , cancer research , cell growth , oncogene , biology , cell cycle , moesin , cell , cell culture , ezrin , transfection , in vivo , biochemistry , genetics , cytoskeleton , microbiology and biotechnology
Increasing evidence has demonstrated that ezrin-radixin-moesin (ERM)-binding phosphoprotein 50 (EBP50) is involved in the malignant transformation of numerous human cancers. The present study investigated the involvement of EBP50 overexpression in the tumorigenicity of pancreatic cancer (PC). The results revealed that overexpression of EBP50 suppressed cell growth, promoted cell apoptosis and arrested G1-to-S phase progression in two human PC cell lines. Overexpression of EBP50 also suppressed B-cell lymphoma 2 (Bcl-2) expression. Furthermore, nude mouse tumor xenograft models were established by the subcutaneous injection of cell lines stably transfected with an EBP50-expressing plasmid. The in vivo data indicated that overexpression of EBP50 inhibited the growth of the PC tumors and induced cell apoptosis. Thus, the present study demonstrated that EBP50 overexpression induces growth inhibition and apoptosis in PC by decreasing Bcl-2 expression. The results suggest that EBP50 may function as a potential tumor suppressor in vivo and in vitro .
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