Key result
Ginsenoside Rg3 inhibited hypoxia-induced VEGF expression, cell proliferation, and multiple signaling pathways (HIF-1α, COX-2, NF-κB, STAT3, ERK1/2, JNK) in human cancer cells.
Why the study?
Does Ginsenoside Rg3 inhibit hypoxia-induced VEGF expression in human cancer cells?
Does Ginsenoside Rg3 inhibit hypoxia-induced VEGF expression in human cancer cells?
Ginsenoside Rg3 down-regulates VEGF expression in cancer cells by targeting multiple hypoxia-induced signaling pathways, providing a mechanistic basis for its anti-angiogenic and anti-tumor efficacy.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for anti-angiogenic effects in cancer; leaves open clinical translation pending human trials.
AIMS: The 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. METHODS: MTT 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. RESULTS: Rg3 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. CONCLUSIONS: Rg3 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.
No takes yet. Share an insight, caveat, or question.
Chen et al. (2010) studied Human esophageal carcinoma and renal cell carcinoma (Eca-109 and 786-0 cells). Ginsenoside Rg3 was evaluated on VEGF expression, cell proliferation, and signaling pathway activation. Ginsenoside Rg3 inhibited hypoxia-induced VEGF expression, cell proliferation, and multiple signaling pathways (HIF-1α, COX-2, NF-κB, STAT3, ERK1/2, JNK) in human cancer cells.
Synapse has enriched 10 related papers. Consider them for comparative context: