期刊
CELLULAR SIGNALLING
卷 24, 期 8, 页码 1531-1540出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2012.03.015
关键词
Paxillin; Phospholipase D; Erk; Breast cancer
类别
资金
- NIGMS from the National Institutes of Health [S06-GM606564]
- National Science Foundation [0346975]
- National Center for Research Resources [G12RR003037]
- National Institute on Minority Health and Health Disparities of the National Institutes of Health [8G12MD007599]
- Div Of Molecular and Cellular Bioscience
- Direct For Biological Sciences [0346975] Funding Source: National Science Foundation
MDA-MB-231 cells are highly aggressive human breast adenocarcinoma cells that depend on PLD activity for survival. In response to the stress of serum withdrawal, there is increased motility and invasiveness of these cells that is associated with a rapid increase in PLD activity. In addition, PLD activity is elevated in response to most mitogenic signals. Similar to PLD, paxillin, a focal adhesion adaptor protein, and Erk, mitogen-activated protein kinase, play vital roles in cell motility through regulation of focal adhesion dynamics. Here, we addressed whether there is a functional correlation between paxillin and PLO that may influence cancer cell motility. We investigated the role of PLD activity on paxillin regulation. Erk activation and formation of a paxillin-Erk and paxillin-FAK association. Inhibition of PLD activity led to an increase in paxillin tyrosine phosphorylation, a decrease in Erk activation, as measured by phosphorylation, and enhanced association of paxillin with Erk. In addition, we found that paxillin tyrosine phosphorylation depends upon Erk activity and may be a consequence of an increased association with FAK. Taken together, these results suggest that Erk activity is governed by PLD activity and regulates the tyrosine phosphorylation of paxillin, potentially explaining its role in cell motility. This study indicated that PLD, Erk, paxillin and FAK participate in the same signaling pathway in this breast cancer cell line. (C) 2012 Elsevier Inc. All rights reserved.
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