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.