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J. Biol. Chem., Vol. 282, Issue 41, 29919-29926, October 12, 2007

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Stress Hormones Regulate Interleukin-6 Expression by Human Ovarian Carcinoma Cells through a Src-dependent Mechanism^*

Monique B. Nilsson¹, Guillermo Armaiz-Pena¹, Rie Takahashi^¶1, Yvonne G. Lin, Jose Trevino, Yang Li, Nicholas Jennings, Jesusa Arevalo^¶, Susan K. Lutgendorf^||, Gary E. Gallick, Angela M. Sanguino^**, Gabriel Lopez-Berestein^**, Steven W. Cole^¶, and Anil K. Sood²

From the Departments of Cancer Biology, Gynecologic Oncology, and ^**Experimental Therapeutics, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, ^¶Division of Hematology-Oncology, Department of Medicine, University of California Los Angeles School of Medicine, Los Angeles, California 90095, and ^||Department of Psychology, University of Iowa, Iowa City, Iowa 52241

Recent studies have demonstrated that chronic stress promotes tumor growth, angiogenesis, and metastasis. In ovarian cancer, levels of the pro-angiogenic cytokine, interleukin 6 (IL-6), are known to be elevated in individuals experiencing chronic stress, but the mechanism(s) by which this cytokine is regulated and its role in tumor growth remain under investigation. Here we show that stress hormones such as norepinephrine lead to increased expression of IL-6 mRNA and protein levels in ovarian carcinoma cells. Furthermore, we demonstrate that norepinephrine stimulation activates Src tyrosine kinase and this activation is required for increased IL-6 expression. These results demonstrate that stress hormones activate signaling pathways known to be critical in ovarian tumor progression.

Received for publication, December 18, 2006 , and in revised form, June 21, 2007.

^* This work was supported in part by National Institutes of Health Grants CA109298 and CA110793, The Marcus Foundation, the University of Texas M.D. Anderson Cancer Center SPORE in Ovarian Cancer (P50 CA 083639), a Program Project development grant from the Ovarian Cancer Research Fund, Inc., and the Zarrow Foundation. 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.

¹ These authors contributed equally to this work.

² To whom correspondence should be addressed: U. T. M. D. Anderson Cancer Center, 1155 Herman Pressler, Unit 1362, Houston, TX 77030. Tel.: 713-745-5266; Fax: 713-792-7586; E-mail: asood{at}mdanderson.org.

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