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J. Biol. Chem., Vol. 281, Issue 35, 25644-25651, September 1, 2006

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Cyclin D3 Expression in Melanoma Cells Is Regulated by Adhesion-dependent Phosphatidylinositol 3-Kinase Signaling and Contributes to G₁-S Progression^*

From the Center for Cell Biology and Cancer Research, Albany Medical College, Albany, New York 12208

D-type cyclins regulate G₁ cell cycle progression by enhancing the activities of cyclin-dependent kinases (CDKs), and their expression is frequently altered in malignant cells. We and others have previously shown that cyclin D1 is up-regulated in melanoma cells through adhesion-independent MEK-ERK1/2 signaling initiated by mutant B-RAF. Here, we describe the regulation and role of cyclin D3 in human melanoma cells. Cyclin D3 expression was enhanced in a cell panel of human melanoma cell lines compared with melanocytes and was regulated by fibronectin-mediated phosphatidylinositol 3-kinase/Akt signaling but not MEK activity. RNA interference experiments demonstrated that cyclin D3 contributed to G₁-S cell cycle progression and proliferation in melanoma cells. Overexpression of cyclin D1 did not recover the effects of cyclin D3 knockdown. Finally, immunoprecipitation studies showed that CDK6 is a major binding partner for cyclin D3, whereas CDK4 preferentially associated with cyclin D1. Together, these findings demonstrate that cyclin D3 is an important regulator of melanoma G₁-S cell cycle progression and that D-type cyclins are differentially regulated in melanoma cells.

Received for publication, January 9, 2006 , and in revised form, June 12, 2006.

^* This work was supported by National Institutes of Health Grant R01-GM067893. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Fig. 1.

¹ To whom correspondence should be addressed. Tel.: 518-262-5700; Fax: 518-262-5669; E-mail: aplina{at}mail.amc.edu.

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