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Oncol Rep. 2017 Nov;38(5):2985-2992. doi: 10.3892/or.2017.5953. Epub 2017 Sep 13.

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

Author information

1
Department of Oral and Maxillofacial Surgery, School of Dentistry, Chosun University, Gwangju 61452, Republic of Korea.
2
Department of Periodontology, School of Dentistry, Chosun University, Gwangju 61452, Republic of Korea.
3
Department of Prosthodontics, School of Dentistry, Chosun University, Gwangju 61452, Republic of Korea.
4
Department of Oral and Maxillofacial Radiology, School of Dentistry, Chosun University, Gwangju 61452, Republic of Korea.
5
Oral Biology Research Institute, School of Dentistry, Chosun University, Gwangju 61452, Republic of Korea.
6
Regional Innovation Center for Dental Science and Engineering, School of Dentistry, Chosun University, Gwangju 61452, Republic of Korea.

Abstract

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 receptor mediated-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.

PMID:
28901495
DOI:
10.3892/or.2017.5953
[Indexed for MEDLINE]

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