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王树林

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Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth

王树林Peiwen Fei Wenge Wang Seok-hyun Kim Shulin Wang Timothy F. Burns Joanna K. Sax Monica Buzzai David T. Dicker W. Gillies McKenna Eric J. Bernhard and Wafik S. El-Deiry*

CANCER CELL, 2004, 6: 597-609,-0001,():

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摘要/描述

p53-dependent apoptosis is a major determinant of its tumor suppressor activity and can be triggered by hypoxia. No p53 target is known to be induced by p53 or to mediate p53-dependent apoptosis during hypoxia. We report that p53 can directly upregulate expression of Bnip3L, a cell death inducer. During hypoxia, Bnip3L is highly induced in wild-type p53-expressing cells, in part due to increased recruitment of p53 and CBP to Bnip3L. Apoptosis is reduced in hypoxia-exposed cells with functional p53 following Bnip3L knockdown. In vivo, Bnip3L knockdown promotes tumorigenicity of wild-type versus mutant p53-expressing tumors. Thus, Bnip3L, capable of attenuating tumorigenicity, mediates p53-dependent apoptosis under hypoxia, which provides a novel understanding of p53 in tumor suppression.

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【免责声明】以下全部内容由[王树林]上传于[2009年12月09日 17时53分11秒],版权归原创者所有。本文仅代表作者本人观点,与本网站无关。本网站对文中陈述、观点判断保持中立,不对所包含内容的准确性、可靠性或完整性提供任何明示或暗示的保证。请读者仅作参考,并请自行承担全部责任。

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