Abstract Title:

Apigenin inhibited migration and invasion of human ovarian cancer A2780 cells through focal adhesion kinase.

Abstract Source:

Carcinogenesis. 2008 Dec;29(12):2369-76. Epub 2008 Oct 28. PMID: 18974065

Abstract Author(s):

Xiao-Wen Hu, Dan Meng, Jing Fang

Article Affiliation:

Key Laboratory of Nutrition and Metabolism, Institute of Nutritional Sciences, Shanghai Institute for Biological Sciences, The Graduate School of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.


Apigenin, a common dietary flavonoid, has been found to have antitumor properties and therefore poses special interest for the development of chemopreventive and/or chemotherapeutic agent for cancers. Here, we demonstrate that apigenin inhibits expression of focal adhesion kinase (FAK) and migration and invasion of human ovarian cancer A2780 cells. FAK is a non-receptor protein tyrosine kinase downstream of integrins and growth factors. It plays an important role in migration and invasion of cancer cells. We found that apigenin inhibited adhesion, migration and invasion of A2780 cells. Apigenin attenuated FAK expression through reducing its protein stability. FAK plays a critical role in migration and invasion of A2780 cells. Overexpression of FAK could reverse A2780 cell migration and invasion inhibited by apigenin. The in vivo experiments showed that apigenin inhibited spontaneous metastasis of A2780 cells implanted onto the ovary of nude mice. Our results provide a new insight into the mechanisms that apigenin inhibits ovarian cancers. These results suggest that molecular targeting of FAK by apigenin might be a useful strategy for chemoprevention and/or chemotherapeutics of ovarian cancers.

Study Type : In Vitro Study

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