• Qing-Jiang Chen, Ming-Zhi Zhang, and Le-Xin Wang.
• Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou City.
• Cell. Physiol. Biochem. 2010 Jan 1; 26 (6): 849-58.

AimsThe ginsenoside Rg3 (Rg3) inhibits xenograft growth and angiogenesis in tumors mainly via down-regulates VEGF expression. This study was designed to investigate the mechanisms by which Rg3 down-regulates VEGF expression.MethodsMTT assay was performed to investigate the effect of Rg3 on the growth of human esophageal carcinoma cell line Eca-109 and 786-0 cells under normoxic and hypoxic conditions. ELISA was used to detect VEGF protein secreted by the cells under normoxic and hypoxic conditions. Real-time quantitative reverse transcriptase polymerase chain reaction and Western blotting were used to detect gene expression and protein synthesis.ResultsRg3 inhibited Eca-109 and 786-0 cell proliferation and induced a significant reduction in VEGF mRNA under hypoxia conditions. Rg3 treatment inhibited hypoxia-induced expression HIF-1α, COX-2 and NF-κB under normoxic and hypoxic conditions. Treatment with Rg3 reduced the hypoxia-induced phosphorylation of STAT3 in a dose-dependent manner in the both cell lines. Rg3 treatment also inhibited the phosphorylation of ERK1/2 and JNK induced by hypoxia.ConclusionsRg3 targets hypoxia-induced multiple signaling pathways to down-regulate VEGF expression in cancer cells. These actions may contribute to the overall efficacy of Rg3 against tumor angiogenesis and growth.Copyright © 2010 S. Karger AG, Basel.

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