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Molecular Biology and Genetics |
Cell Cycle Laboratory [P. M. O., M. T., T. P. M.] and Molecular/Cancer Biology Laboratory [T. V.], Haartman Institute, 00014 University of Helsinki, Helsinki, Finland; Department of Oncology, University of Helsinki, and Helsinki University Central Hospital, 00029 HYKS, Helsinki, Finland [P. S.]; Immunopathology Laboratory, Institute for Pathology and Oncology, Karolinska Institute/Hospital, S-171 76 Stockholm, Sweden [E. C-V., P. B.]; and Department of Pathology and Division of Epidemiology, Columbia University College of Physicians and Surgeons, New York, New York 10032 [R. S.]
Kaposi’s sarcoma-associated herpesvirus (KSHV) has a key etiological role in development of Kaposi’s sarcoma (KS). v-Cyclin is a KSHV-encoded homologue to D-type cyclins that associates with cellular cyclin-dependent kinase 6 (CDK6). v-Cyclin promotes S-phase entry of quiescent cells and has been suggested to execute functions of both D- and E-type cyclins. In this study, expression of v-cyclin in cells with elevated levels of CDK6 led to apoptotic cell death after the cells entered S phase. The cell death required the kinase activity of CDK6 because cells expressing a kinase-deficient form of CDK6 did not undergo apoptosis upon v-cyclin expression. Studies on the mechanisms involved in this caspase-3-mediated apoptosis indicated that it was independent of cellular p53 or pRb status, and it was not suppressed by Bcl-2. In contrast, the KSHV-encoded v-Bcl-2 efficiently suppressed v-cyclin-/CDK6-induced apoptosis, demonstrating a marked difference in the antiapoptotic properties of c-Bcl-2 and v-Bcl-2. In KS lesions, high CDK6 expression was confined to a subset of cells, some of which displayed signs of apoptosis. These results suggest that v-cyclin may exert both growth-promoting and apoptotic functions in KS, depending on factors regulating CDK6 and v-Bcl-2 levels.
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