期刊
ONCOGENE
卷 24, 期 4, 页码 672-679出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1208099
关键词
phospholipase D; survival signals; rapamycin; phosphatidylinositol-3-kinase; Akt; breast cancer
资金
- NCI NIH HHS [CA46677] Funding Source: Medline
- NCRR NIH HHS [RR03037] Funding Source: Medline
- NIGMS NIH HHS [GM60654] Funding Source: Medline
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.
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