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J. Biol. Chem., Vol. 276, Issue 43, 39903-39910, October 26, 2001

This Article Full Text Full Text (PDF) All Versions of this Article: 276/43/39903    most recent M010281200v1 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zhao, X. Articles by Yokoyama, K. K. Search for Related Content PubMed PubMed Citation Articles by Zhao, X. Articles by Yokoyama, K. K. Social Bookmarking                      What's this?

Protein Kinase C Plays a Critical Role in Mannosylerythritol Lipid-induced Differentiation of Melanoma B16 Cells^*

Xiaoxian Zhao^§, Takehide Murata, Shigeo Ohno^¶, Noel Day, Jun Song, Nobuhiko Nomura^§, Tadaatsu Nakahara^§, and Kazunari K. Yokoyama

From the  RIKEN, Tsukuba Institute, Ibaraki 305-0074, Japan; the ^§ Institute of Applied Biochemistry, University of Tsukuba, Ibaraki 305-0006, Japan; and the ^¶ Department of Molecular Biology, Yokohama City University, School of Medicine, 3-9 Fuku-ura, Kanazawa-Ku, Yokohama 236-0004, Japan

Mannosylerythritol lipid (MEL), a novel extracellular glycolipid from yeast, was found to inhibit the proliferation of mouse melanoma B16 cells in a dose-dependent manner and to induce the apoptosis of B16 cells at concentrations higher than 10 µM (Zhao, X., Wakamatsu, Y., Shibahara, M., Nomura, N., Geltinger, C., Nakahara, T., Murata, T., and Yokoyama, K. K. (1999) Cancer Res. 59, 482-486). We show here that exposure of B16 cells to MEL (5 µM) for 2 days resulted in an increase of the levels of differentiation-associated markers of melanoma cells such as melanogenesis and tyrosinase activity, which were accompanied by morphological changes. The MEL-induced differentiation of B16 cells at this concentration was closely associated with arrest of the cell cycle at G₁ phase, but no significant population of apoptotic cells was identified. Expression of protein kinase C (PKC) was enhanced after exposure of B16 cells to MEL for 48 h. Antisense oligodeoxynucleotides against the mouse gene for PKC prevented MEL-induced melanogenesis in B16 cells. Conversely, the effects of the expression of a constitutively active form of PKC mimicked the effects of MEL on B16 cells. These data suggest that MEL, a yeast-derived glycolipid, triggers the differentiation of B16 melanoma cells through a signaling pathway that involves PKC.

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