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J. Biol. Chem., Vol. 283, Issue 20, 13506-13509, May 16, 2008

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Requirement of Inositol 1,4,5-Trisphosphate Receptors for Tumor-mediated Lymphocyte Apoptosis^*

Camia Steinmann, Megan L. Landsverk, José M. Barral, and Darren Boehning¹

From the Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas 77555-0620 and the Department of Pediatrics, University of Washington, Seattle, Washington 98195-6320

Tumor cells strategically down-regulate Fas receptor expression to evade immune attack and up-regulate expression of Fas ligand to promote apoptosis of infiltrating T lymphocytes. Many pathways leading to apoptotic cell death require calcium release from inositol 1,4,5-trisphosphate receptors (IP₃Rs). Here, we show that Fas-dependent killing of Jurkat T lymphoma cells by SW620 colon cancer cells requires calcium release from IP₃R. General suppression of IP₃R signaling significantly reduced SW620-mediated Jurkat cell apoptosis. Significantly, a specific inhibitor of apoptotic calcium release from IP₃R strongly blocked lymphocyte apoptosis. Thus, selective pharmacological targeting of apoptotic calcium release from IP₃R may enhance tumor cell immunogenicity.

Received for publication, February 7, 2008 , and in revised form, March 24, 2008.

^* This work was supported, in whole or in part, by National Institutes of Health Grant GM081685 (to D. B.). This work was also supported by the University of Texas Medical Branch. 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 To whom correspondence should be addressed: 301 University Blvd., University of Texas Medical Branch, Galveston, TX, 77555-0620. Fax: 409-747-2200; E-mail: dfboehni{at}utmb.edu.

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