Alternative phospholipase D/mTOR survival signal in human breast cancer cells

被引：87

作者：

Chen, YH ^{[1
]}

Rodrik, V ^{[1
]}

Foster, DA ^{[1
]}

机构：

[1] CUNY Hunter Coll, Dept Biol Sci, New York, NY 10021 USA

来源：

ONCOGENE | 2005年 / 24卷 / 04期

关键词：

phospholipase D; survival signals; rapamycin; phosphatidylinositol-3-kinase; Akt; breast cancer;

D O I：

10.1038/sj.onc.1208099

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Cancer cells generate survival signals to suppress default apoptotic programs that protect from cancer. Phosphatidylinositol-3-kinase (PI3K) generates a survival signal that is frequently dysregulated in human cancers. Phospholipase D (PLD) has also been implicated in signals that promote survival. One of the targets of PLD signaling is mTOR ( mammalian target of rapamycin), a critical regulator of cell cycle progression and cell growth. We report here that elevated PLD activity in the MDA-MB-231 human breast cancer cell line generates an mTOR-dependent survival signal that is independent of PI3K. In contrast, MDA-MB-435S breast cancer cells, which have very low levels of PLD activity, are dependent on PI3K for survival signals. The data presented here identify an alternative survival signal that is dependent on PLD and mTOR and is active in a breast cancer cell line where the PI3K survival pathway is not active.

引用

页码：672 / 679

页数：8

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