This Article Full Text Full Text (PDF) All Versions of this Article: 147/1/530    most recent Author Manuscript (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Enomoto, M. Articles by Park, M. K. Search for Related Content PubMed PubMed Citation Articles by Enomoto, M. Articles by Park, M. K. Pubmed/NCBI databases Compound via MeSH Substance via MeSH

Gonadotropin-Releasing Hormone Induces Actin Cytoskeleton Remodeling and Affects Cell Migration in a Cell-Type-Specific Manner in TSU-Pr1 and DU145 Cells

Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Bunkyo, Tokyo 113-0033, Japan

Address all correspondence and requests for reprints to: Min Kyun Park. Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-0033, Japan. E-mail: biopark{at}biol.s.u-tokyo.ac.jp.

GnRH was first identified as the hypothalamic decapeptide that promotes gonadotropin release from pituitary gonadotropes. Thereafter, direct stimulatory and inhibitory effects of GnRH on cell proliferation were demonstrated in a number of types of primary cultured cells and established cell lines. Recently, the effects of GnRH on cell attachment, cytoskeleton remodeling, and cell migration have also been reported. Thus, the effects of GnRH on various cell activities are of great interest among researchers who study the actions of GnRH. In this study, we demonstrated that GnRH induces actin cytoskeleton remodeling and affects cell migration using two human prostatic carcinoma cell lines, TSU-Pr1 and DU145. In TSU-Pr1, GnRH-I and -II induced the filopodia formation of the cells and promoted cell migration, whereas in DU145, GnRH-I and -II induced the formation of the cells with stress fiber and inhibited cell migration. In our previous studies, we reported the stimulatory and inhibitory effects of GnRH on the cell proliferation of TSU-Pr1 and DU145 cells. This study provides the first evidence for the effects of GnRH on actin cytoskeleton remodeling and cell migration of cells in which cell proliferation was affected by GnRH at the same time. Moreover, we also demonstrated that the same human GnRH receptor subtype, human type I GnRH receptor, is essential for the effects of GnRH-I and -II on actin cytoskeleton remodeling and cell migration in both TSU-Pr1 and DU145 cells using the technique of gene knock-down by RNA interference.

This article has been cited by other articles:

				A. M. Navratil, J. G. Knoll, J. D. Whitesell, S. A. Tobet, and C. M. Clay Neuroendocrine Plasticity in the Anterior Pituitary: Gonadotropin-Releasing Hormone-Mediated Movement in Vitro and in Vivo Endocrinology, April 1, 2007; 148(4): 1736 - 1744. [Abstract] [Full Text] [PDF]

				L. W.T. Cheung, P. C.K. Leung, and A. S.T. Wong Gonadotropin-Releasing Hormone Promotes Ovarian Cancer Cell Invasiveness through c-Jun NH2-Terminal Kinase-Mediated Activation of Matrix Metalloproteinase (MMP)-2 and MMP-9. Cancer Res., November 15, 2006; 66(22): 10902 - 10910. [Abstract] [Full Text] [PDF]