Apigenin induces apoptosis via tumor necrosis factor receptor- and Bcl-2-mediated pathway and enhances susceptibility of head and neck squamous cell carcinoma to 5-fluorouracil and cisplatin

doi:10.1016/j.bbagen.2012.04.013

CNU IR > Pharmacy and Science > Dept. of Cosmetic Science and institute of cosmetic science > Periodical Articles > Item 310902800/27618

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/27618

Title:	Apigenin induces apoptosis via tumor necrosis factor receptor- and Bcl-2-mediated pathway and enhances susceptibility of head and neck squamous cell carcinoma to 5-fluorouracil and cisplatin
Authors:	Chan, Leong-Perng Chou, Tzung-Han Ding, Hsiou-Yu Chen, Pin-Ru Chiang, Feng-Yu Kuo, Po-Lin Liang, Chia-Hua
Contributors:	化妝品應用與管理系
Keywords:	Apigenin Human Head And Neck Squamous Cell Carcinoma Death Receptor 5-Fluorouracil Cisplatin
Date:	2012-07
Issue Date:	2014-03-21 16:15:25 (UTC+8)
Publisher:	Elsevier Science Bv
Abstract:	Background: Apigenin, a natural plant flavone, may have chemopreventive and therapeutic potentials for anti-inflammatory, antioxidant, and anti-cancer. Nevertheless, the anti-tumor effect of apigenin on human head and neck squamous cell carcinoma (HNSCC) is not fully understood.Methods: The antioxidant capacity and protective effects of apigenin against oxidative stress in murine normal embryonic liver BNLCL2 cells are examined. Cell viability, morphologic change, clonogenic survival, cell cycle distribution, reactive oxygen species (ROS) production, glutathione formation, and death receptors- and Bcl-2-mediated caspase pathways of HNSCC SCC25 cells and A431 cells with apigenin are investigated.Results: Apigenin inhibits the growth of SCC25 and A431 cells and induces cell cycle arrest in the G(2)/M phase. Apigenin has an antioxidant capacity as well as the ability to inhibit lipid peroxidation. It protects BNLCL2 cells against oxidative damage, and is potentially able to prevent cancer. Apigenin increases intracellular ROS levels and reduces levels of glutathione; it also induces cell apoptosis via tumor necrosis factor receptor (TNF-R)-, TNF-related apoptosis-inducing ligand receptor (TRAIL-R)-, and Bcl-2-mediated caspase-dependent cell death pathways in SCC25 cells. The combination of apigenin with 5-fluorouracil (5-Fu) or cisplatin induces the dramatic death of SCC25 cells.Conclusions: Apigenin induces SCC25 cell apoptosis via the up-regulation of both TNF-R and TRAIL-R signaling pathways, and has a synergistic effect on the inhibition of cell proliferation in combination with 5-Fu or cisplatin.General significance: These analytical findings suggest that apigenin may be a good therapeutic agent against HNSCC cells. (C) 2012 Elsevier B.V. All rights reserved.
Relation:	Biochimica Et Biophysica Acta-General Subjects, 1820(7), 1081-1091
Appears in Collections:	[Dept. of Cosmetic Science and institute of cosmetic science] Periodical Articles

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