Apigenin Inhibits Expression of Vascular Endothelial Growth Factor and Angiogenesis in Human Lung Cancer Cells: Implication of Chemoprevention of Lung Cancer

  title={Apigenin Inhibits Expression of Vascular Endothelial Growth Factor and Angiogenesis in Human Lung Cancer Cells: Implication of Chemoprevention of Lung Cancer},
  author={Ling-Zhi Liu and Jing Fang and Qiong Zhou and Xiaowen Hu and Xianglin Shi and Bing-Hua Jiang},
  journal={Molecular Pharmacology},
  pages={635 - 643}
Apigenin is a natural dietary flavonoid. It has recently been shown to have anticancer effects on prostate and ovarian cancer cells. However, the molecular basis of the effect of apigenin on cancer cells remains to be elucidated. In this study, we found that apigenin inhibited A549 lung cancer cell proliferation and vascular endothelial growth factor (VEGF) transcriptional activation in a dose-dependent manner. In an attempt to understand the mechanism of apigenin-inhibited VEGF expression, we… 

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The results identify apigenin as a bioflavonoid that inhibits hypoxia‐activated pathways linked to cancer progression in human prostate cancer, in particular the PI3K/Akt/GSK‐3 pathway.

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9-β-d-Arabinofuranosyl-2-fluoroadenine Inhibits Expression of Vascular Endothelial Growth Factor through Hypoxia-Inducible Factor-1 in Human Ovarian Cancer Cells

A new function of Fara-A is demonstrated in inhibiting VEGF and HIF-1α expression and a potential molecular mechanism of the regulation is identified.

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The results suggest that apigenin is a promising antibreast cancer agent and its growth inhibitory effects are mediated by targeting different signal transduction pathways in MCF-7 and MDA-MB-468 breast carcinoma cells.

Molecular mechanisms for apigenin‐induced cell‐cycle arrest and apoptosis of hormone refractory human prostate carcinoma DU145 cells

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It is demonstrated that arsenite induces the expression of Hif-1α but not HIF-1β subunit in DU145 human prostate carcinoma cells, indicating that the arsenite-induced activation of PI3K/Akt signaling and theexpression of H IF-1 and VEGF through the generation of ROS could be an important mechanism in the arsenITE-induced carcinogenesis.

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