期刊
CANCER CELL
卷 22, 期 5, 页码 615-630出版社
CELL PRESS
DOI: 10.1016/j.ccr.2012.09.027
关键词
-
资金
- Breast Cancer Research Foundation
- NIGMS Cell Migration Consortium
- NIH [P01 HL059561, GM61010, GM58801]
- UCSF/UC Berkeley Nanomedicine Development Center
- National Science Foundation
- Lee Jeans Foundation through the Entertainment Industry Foundation
Dynamic actin cytoskeletal reorganization is integral to cell motility. Profilins are well-characterized regulators of actin polymerization; however, functional differences among coexpressed profilin isoforms are not well defined. Here, we demonstrate that profilin-1 and profilin-2 differentially regulate membrane protrusion, motility, and invasion; these processes are promoted by profilin-1 and suppressed by profilin-2. Compared to profilin-1, profilin-2 preferentially drives actin polymerization by the Ena/VASP protein, EVL. Profilin-2 and EVL suppress protrusive activity and cell motility by an actomyosin contractility-dependent mechanism. Importantly, EVL or profilin-2 downregulation enhances invasion in vitro and in vivo. In human breast cancer, lower EVL expression correlates with high invasiveness and poor patient outcome. We propose that profilin-2/EVL-mediated actin polymerization enhances actin bundling and suppresses breast cancer cell invasion.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据