Abstract

Abstract Osteosarcoma is the most common primary malignant bone tumor. Angiogenesis is essential for the tumor growth. Angiopoietin-2 (Angpt2) plays a critical role in angiogenesis and tumor progression. Connective tissue growth factor (CTGF), a secreted protein that binds to integrins, modulates the angiogenesis of certain human cancer cells. However, the effect of CTGF on Angpt2 expression in human osteosarcoma cells is mostly unknown. In this study, we found that overexpression of CTGF in osteosarcoma promoted angiogenesis in vitro and in vivo by tube formation assay, and Matrigel plug assay. Knockdown of CTGF obviously reduced expression of Angpt2 and angiogenesis. Recently, microRNAs (miRNAs) have been demonstrated that functions as oncogenes or angiogenesis regulators in human cancer. Here, we also found that overexpression of CTGF significantly decreased miR-543 in osteosarcoma cells. Transfection of miR-543 mimic reduced Angpt2 expression and angiogenesis. Taken together, CTGF promotes angiogenesis via up-regulation of Angpt2 by decreasing miR-543 in human osteosarcoma. These findings certify that CTGF functions as a tumor enhancer gene, suggesting that CTGF may be a potential therapeutic target for osteosarcoma patients. Citation Format: Yu-che Cheng, Hsiao-Chi Tsai, Tzu-Wei Tan, Chih-Hsin Tang. CTGF promotes tumor angiogenesis process in osteosarcoma through induction of angiopoietin-2. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3399.

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