Abstract
Abstract Leptin, the product of the obese gene that plays an important role in the regulation of body weight that induces neuroprotection, neurogenesis, and angiogenesis. However, the effect of leptin on VEGF expression in human chondrosarcoma cells is mostly unknown. The aim of study is try to examine the effect of leptin in VEGF expression and angiogenesis in human chondrosarcoma cells. We found that exogenous leptin with chondrosarcoma cells promoted VEGF expression and subsequently increased migration and tube formation in endothelial progenitor cells (EPC). Leptin-mediated VEGF and angiogenesis up-regulation were attenuated by OBRl receptor antisense oligonucleotide. In addition, leptin-induced VEGF expression was attenuated by ERK inhibitor (U0126), p38 inhibitor (SB203580), JNK inhibitor (SP600125) and AP-1 inhibitors (Curcumin and Tanshinone). Incubation of cells with leptin induced ERK, p38, JNK and c-Jun phosphorylation as well as AP-1 luciferase activity. Knockdown of leptin decreased VEGF expression and also abolished chondrosarcoma conditional medium-mediated angiogenesis in vitro as well as angiogenesis effects in the matrigel plug model in vivo. In addition, using xenograft tumor angiogenesis model, knockdown leptin significantly reduced tumor growth and tumor angiogenesis. Taken together, our results indicated that leptin enhances the VEGF expression in chondrosarcoma cells. One of the mechanisms underlying leptin-directed VEGF expression was through the ERK/p38/JNK and c-Jun signal transduction pathway. Citation Format: Kai-Hsiang Hsu, Chih-Hsin Tang, Tzu-Wei Tan. Leptin increases VEGF expression and enhances angiogenesis in human chondrosarcoma cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1005. doi:10.1158/1538-7445.AM2014-1005
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