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Prepublished online as a Blood First Edition Paper on January 16, 2003; DOI 10.1182/blood-2002-07-1994. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-07-1994v1 101/10/4070    most recent 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 Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lundquist, A. Articles by Coqueret, O. Search for Related Content PubMed PubMed Citation Articles by Lundquist, A. Articles by Coqueret, O. Related Collections Neoplasia Cell Cycle Oncogenes and Tumor Suppressors Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 May 2003, Vol. 101, No. 10, pp. 4070-4077 NEOPLASIA Kaposi sarcoma-associated viral cyclin K overrides cell growth inhibition mediated by oncostatin M through STAT3 inhibition Amy Lundquist, Benjamin Barré, Frédéric Bienvenu, Jacques Hermann, Sylvie Avril, and Olivier Coqueret From the Institut National de la Santé et de la Recherche Médicale (INSERM) U564, Angers, France. DNA viruses have evolved a number of mechanisms to inhibit the major cellular tumor-suppressor pathways. Viral oncogenes can override growth suppressive signals and extend the virus proliferative capacity. The Kaposi sarsoma-associated human herpesvirus 8 (KSHV) encodes a protein, cyclin K, that is similar to cellular cyclin D1 but behaves atypically. Cyclin K resists the actions of the p16 INK4a and p27Kip1 inhibitors and extends the range of cdk6 substrates, thereby inducing cell-cycle progression toward S phase. In this study, we show that cyclin K overrides growth suppressive signals through signal transducer and activator of transcription 3 (STAT3) inactivation. Cyclin K was found to associate with the activation domain of STAT3 to inhibit its DNA-binding and transcriptional activities. Overexpression of cyclin K and inhibition of STAT3 prevents the growth suppressive effect imposed by the interleukin 6-type cytokine, oncostatin M. Altogether, these results suggest that KSHV is able to override growth suppressive effects through multiple mechanisms, and they further indicate that cyclin K plays an important role in the oncogenic activity of these viruses. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: V. L. Tarakanova, F. Kreisel, D. W. White, and H. W. Virgin IV Murine Gammaherpesvirus 68 Genes both Induce and Suppress Lymphoproliferative Disease J. Virol., January 15, 2008; 82(2): 1034 - 1039. [Abstract] [Full Text] [PDF] P.-C. Chang and M. Li Kaposi's Sarcoma-Associated Herpesvirus K-Cyclin Interacts with Cdk9 and Stimulates Cdk9-Mediated Phosphorylation of p53 Tumor Suppressor J. Virol., January 1, 2008; 82(1): 278 - 290. [Abstract] [Full Text] [PDF] J. W. Upton and S. H. Speck Evidence for CDK-Dependent and CDK-Independent Functions of the Murine Gammaherpesvirus 68 v-Cyclin J. Virol., December 15, 2006; 80(24): 11946 - 11959. [Abstract] [Full Text] [PDF]

	Copyright © 2003 by American Society of Hematology         Online ISSN: 1528-0020