Inhibition of invasiveness of human lung cancer cell line H1299 by over-expression of cofilin

• Published in: Cell biology international 2005-11, Vol.29 (11), p.877-883
• Main Authors: Lee, Yi-Jang, Mazzatti, Dawn J., Yun, Zhong, Keng, Peter C.
• Format: Article
• Language: English
• Subjects: Actin cytoskeleton; Actins - chemistry; Blotting, Western; Cancer cell invasion; Cell Line, Tumor; Cell Movement; Cofilin; Cofilin 1 - biosynthesis; Cyclin-Dependent Kinase Inhibitor p27 - metabolism; Doxycycline - pharmacology; Fluorescent Antibody Technique, Indirect; Gene Expression Regulation, Neoplastic; Genes, Reporter; Humans; Lung Neoplasms - drug therapy; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Microscopy, Fluorescence; Neoplasm Invasiveness; p27 kip1; p27kip1; Plasmids - metabolism; Time Factors; Transfection; Ubiquitin - chemistry
• ISSN: 1065-6995; 1095-8355
• DOI: 10.1016/j.cellbi.2005.07.005

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.