作者: Yang Liu , Liang Wang , Xu-Yong Lin , Jian Wang , Juan-Han Yu
DOI: 10.1007/S13277-012-0493-1
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摘要: Accumulating evidence reveals that aberrant expression of claudins manifests in various tumors; however, their biological functions are poorly understood. Here, we report on the elevated claudin-1 human breast cancer MCF-7 cells under tumor necrosis factor (TNF)-α treatment. Interestingly, increased contributes to an anti-apoptotic role TNF-α-induced apoptosis. In line with this, upon TNF-α stimulus, downregulation by siRNA knockdown results a significant increase cleavage caspase-8 and poly (ADP-ribose) polymerase, decrease cyclinD1 expression, DNA fragmentation. Consistently, TdT-mediated dUTP nick end labeling assay also shows loss increases susceptibility However, there is no obvious effect Bax p53 after treatment aforementioned. addition, amount cytoplasmic accumulation β-catenin, while β-catenin cell membrane as well E-cadherin cytoplasm. conclusion, our data reveal novel regulating apoptosis cells.