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Inhibition of invasiveness of human lung cancer cell line H1299 by over‐expression of cofilin
Author(s) -
Lee YiJang,
Mazzatti Dawn J.,
Yun Zhong,
Keng Peter C.
Publication year - 2005
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2005.07.005
Subject(s) - lung cancer , cancer research , cell culture , biology , cofilin , expression (computer science) , microbiology and biotechnology , line (geometry) , cancer , cell , oncology , medicine , genetics , computer science , geometry , mathematics , programming language , actin cytoskeleton , cytoskeleton
The Rho—LIM‐kinase (LIMK) signaling pathway, believed to be involved in the regulation of tumor invasion, specifically regulates the activity of cofilin. However, it is unclear whether cofilin plays a pivotal role in tumor invasiveness. In this paper we show using a tet ‐on gene expression system that over‐expression of cofilin inhibits the invasiveness of human lung cancer H1299 cells. Over‐expressed cofilin disrupts the actin cytoskeleton at the leading edge of the cell and up‐regulates p27 kip1 , which is known to be involved in regulating cell motility. Removal of cofilin over‐expression normalizes the p27 kip1 level and concomitantly restores the invasiveness of the cultured cells. These findings suggest that excessive cofilin production might prevent cancer cell invasion.