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Platelet-Activating Factor Induces Up-regulation of Antiapoptotic Factors in a Melanoma Cell Line through Nuclear Factor-B Activation

¹ Department of Biological Sciences, The Institute of Basic Sciences, Chonnam National University, Kwangju, Republic of Korea and ² Department of Immunology and Research Center for Allergic Immune Diseases, Chonbuk National University Medical School, Chonju, Republic of Korea

Requests for reprints: Suhn-Young Im, Department of Biological Sciences, The Institute of Basic Sciences, Chonnam National University, 500-757 Kwangju, Republic of Korea. Phone: 82-62-530-3414; Fax: 82-62-530-0848; E-mail: syim{at}chonnam.ac.kr.

In this study, we investigated the influence of platelet-activating factor (PAF) on the induction of apoptosis-regulating factors in B16F10 melanoma cells. PAF increased the expression of mRNA and the protein synthesis of antiapoptotic factors, such as Bcl-2 and Bcl-xL, but did not increase the expression of the proapoptotic factor, Bax. A selective nuclear factor-B (NF-B) inhibitor, parthenolide, inhibited the effects of PAF. Furthermore, PAF inhibited etoposide-induced increases in caspase-3, caspase-8, and caspase-9 activities, as well as cell death. p50/p65 heterodimer increased the mRNA expression of Bcl-2 and Bcl-xL and decreased etoposide-induced caspase activities and cell death. In an in vivo model in which Matrigel was injected s.c., PAF augmented the growth of B16F10 cells and attenuated etoposide-induced inhibition of B16F10 cells growth. These data indicate that PAF induces up-regulation of antiapoptotic factors in a NF-B-dependent manner in a melanoma cell line, therefore suggesting that PAF may diminish the cytotoxic effect of chemotherapeutic agents. (Cancer Res 2006; 66(9): 4681-6)

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