Am J Physiol Cell Physiol AJP: Renal Physiology
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Am J Physiol Cell Physiol 297: C451-C458, 2009. First published May 27, 2009; doi:10.1152/ajpcell.00586.2008
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GROWTH, DIFFERENTIATION, AND APOPTOSIS

S1P5 is required for sphingosine 1-phosphate-induced autophagy in human prostate cancer PC-3 cells

Chi-Lun Chang,1 Ming-Chih Ho,3,4 Po-Huang Lee,3,4 Chi-Yen Hsu,1 Wei-Pang Huang,1,2 and Hsinyu Lee1,2

1Institute of Zoology, 2Department of Life Science, and 3Angiogenesis Research Center, National Taiwan University, Taipei, Taiwan, Republic of China; and 4Department of Surgery, National Taiwan University Hospital, Taipei, Taiwan, Republic of China

Submitted 14 November 2008 ; accepted in final form 27 May 2009

Sphingosine 1-phosphate (S1P) is a platelet- and endothelial cell-released lysophospholipid that regulates various cellular functions through activating a specific family of G protein-coupled receptors. Both platelet activation and angiogenesis play important roles in cancer development, implying that cancer cells might encounter a large amount of S1P during these processes. Cancer cells, in the meantime, may experience nutrient deprivation and rely on autophagy for early development. Whether extracellular S1P regulates autophagy remains to be tested. In the present work, we investigated whether autophagy is regulated by S1P in PC-3 cells. Through monitoring the modification patterns of LC3 by Western blotting, we demonstrated that autophagy was induced by exogenously applied S1P in PC-3 cells. This observation was further confirmed by fluorescence microscopy using PC-3 cells stably expressing enhanced green fluorescent protein-LC3. By applying small interfering RNA and dihydro-S1P, S1P5 activation was found to be involved in this process. Besides, mammalian target of rapamycin signaling was inhibited upon S1P treatment. Taken together, our results suggest that, under serum-starved conditions, S1P further upregulates autophagic activity through S1P5-dependent pathways in PC-3 cells.

lysophospholipid; cell survival; autophagosome; mammalian target of rapamycin


Addresses for reprint requests and other correspondence: W.-P. Huang, Dept. of Life Science and Institute of Zoology, National Taiwan Univ., 1 Roosevelt Rd., Section 4, Taipei 106, Taiwan, ROC (e-mail: wphuang{at}ntu.edu.tw) and H. Lee, Dept. of Life Science and Institute of Zoology, National Taiwan Univ., 1 Roosevelt Rd., Section 4, Taipei 106, Taiwan, ROC (e-mail: hsinyu{at}ntu.edu.tw)






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