Abstract Title:

Biochanin-A induces apoptosis and suppresses migration in FaDu human pharynx squamous carcinoma cells.

Abstract Source:

Oncol Rep. 2017 Nov ;38(5):2985-2992. Epub 2017 Sep 13. PMID: 28901495

Abstract Author(s):

In-A Cho, Sang-Joun You, Kyeong-Rok Kang, Su-Gwan Kim, Ji-Su Oh, Jae-Seek You, Gyeong-Je Lee, Yo-Seob Seo, Do Kyung Kim, Chun Sung Kim, Sook-Young Lee, Jae-Sung Kim

Article Affiliation:

In-A Cho


The aim of the present study was to investigate biochanin-A-induced anticancer effects and their cellular signaling pathway in FaDu pharyngeal squamous carcinoma cells. Biochanin-A induced cell death through increased cytotoxicity of FaDu cells in a dose- and time-dependent manner. The number of cells with nucleus condensation and the apoptotic population were increased in the FaDu cells stimulated with biochanin-A for 24 h. Furthermore, extrinsic apoptotic factors such as FasL and their downstream target caspase-8 were increased and activated in the FaDu cells treated with biochanin-A in a dose-dependent manner. Moreover, biochanin-A decreased the expression of intrinsic anti-apoptotic factors such as Bcl-2 and Bcl-xL, and increased the level and activation of intrinsic apoptotic factors such as Bad and caspase-9. Finally, biochanin-A induced the activation of caspase-3 and Poly(ADP ribose) polymerase (PARP) in FaDu cells. Our results suggest that biochanin-A-induced apoptosis was mediated by death receptormediated-extrinsic and mitochondria-dependent intrinsic apoptotic signaling pathways. Biochanin-A also inhibited wound healing migration and proliferation of FaDu cells via the downregulation and inactivation of matrix metalloproteinase-2 and -9 that are mediated by the suppression of p38, mitogen activated protein kinase (MAPK), NF-κB and Akt cellular signaling pathways. Therefore, these data suggest that the biochanin-A may act as a potential chemotherapeutic compound to treat head and neck cancer.

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