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Originally published In Press as doi:10.1074/jbc.M202652200 on August 29, 2002

J. Biol. Chem., Vol. 277, Issue 51, 50087-50097, December 20, 2002
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Impaired Trafficking of Connexins in Androgen-independent Human Prostate Cancer Cell Lines and Its Mitigation by alpha -Catenin*

Rajgopal Govindarajan, Sumin Zhao, Xiao-Hong Song, Rong-Jun Guo, Margaret WheelockDagger , Keith R. JohnsonDagger , and Parmender P. Mehta§

From the Department of Biochemistry and Molecular Biology, Department of Oral Biology and the Dagger  Eppley Cancer Institute, University of Nebraska Medical Center, Omaha, Nebraska 68198

Gap junctions, composed of connexins, provide a pathway of direct intercellular communication for the diffusion of small molecules between cells. Evidence suggests that connexins act as tumor suppressors. We showed previously that expression of connexin-43 and connexin-32 in an indolent prostate cancer cell line, LNCaP, resulted in gap junction formation and growth inhibition. To elucidate the role of connexins in the progression of prostate cancer from a hormone-dependent to -independent state, we introduced connexin-43 and connexin-32 into an invasive, androgen-independent cell line, PC-3. Expression of these proteins in PC-3 cells resulted in intracellular accumulation. Western blot analysis revealed a lack of Triton-insoluble, plaque-assembled connexins. In contrast to LNCaP cells, connexins could not be cell surface-biotinylated and did not reside in the cell surface derived endocytic vesicles, in PC-3 cells, suggesting impaired trafficking to the cell surface. Intracellular accumulation of connexins was observed in several androgen-independent prostate cancer cell lines. Transient expression of alpha -catenin facilitated the trafficking of both connexins to the cell surface and induced gap junction assembly. Our results suggest that impaired trafficking, and not the inability to form gap junctions, is the major cause of communication deficiency in human prostate cancer cell lines.

* This work was supported by National Institutes of Health Grant CA73769 and Department of Defense Grant DAMD-17-00-1-0032.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed: Dept. of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE. Tel.: 402-559-3826; Fax: 402-559-6650; E-mail: pmehta@unmc.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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