Research Article

Dihydromyricetin induces cell apoptosis via a p53-related pathway in AGS human gastric cancer cells

Published: December 02, 2015
Genet. Mol. Res. 14 (4) : 15564-15571 DOI: https://doi.org/10.4238/2015.December.1.7
Cite this Article:
F.J. Ji, X.F. Tian, X.W. Liu, L.B. Fu, Y.Y. Wu, X.D. Fang, H.Y. Jin (2015). Dihydromyricetin induces cell apoptosis via a p53-related pathway in AGS human gastric cancer cells. Genet. Mol. Res. 14(4): 15564-15571. https://doi.org/10.4238/2015.December.1.7
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Abstract

The aim of the present study was to determine the anti­proliferative and pro-apoptotic effects of dihydromyricetin (DHM) on the AGS human gastric cancer cells and their underlying mechanisms. The effects of DHM on AGS cells were evaluated by using 3-(4, 5-di­methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), lactate dehydrogenase, and Annexin V/propidium iodide (PI) double-staining assays. The underlying mechanisms were determined by using quanti­tative real-time polymerase chain reaction. The results demonstrated that DHM significantly (P < 0.05) inhibited AGS cell proliferation and induced cell cytotoxicity in a dose- and time-dependent manner. Ad­ditionally, Annexin V/PI double-staining assay showed that DHM pro­moted cell apoptosis in both, early and late stages. Furthermore, DHM also regulated the expression of apoptotic genes such as p53 and B-cell lymphoma-2 (bcl-2) in a dose- and time-dependent manner. In conclu­sion, this is the first report demonstrating the anticancer and pro-apop­tosis effects of DHM on AGS human gastric cancer cells. The results strongly suggest that DHM may be a potential therapeutic candidate for the treatment of gastric cancer.

The aim of the present study was to determine the anti­proliferative and pro-apoptotic effects of dihydromyricetin (DHM) on the AGS human gastric cancer cells and their underlying mechanisms. The effects of DHM on AGS cells were evaluated by using 3-(4, 5-di­methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), lactate dehydrogenase, and Annexin V/propidium iodide (PI) double-staining assays. The underlying mechanisms were determined by using quanti­tative real-time polymerase chain reaction. The results demonstrated that DHM significantly (P < 0.05) inhibited AGS cell proliferation and induced cell cytotoxicity in a dose- and time-dependent manner. Ad­ditionally, Annexin V/PI double-staining assay showed that DHM pro­moted cell apoptosis in both, early and late stages. Furthermore, DHM also regulated the expression of apoptotic genes such as p53 and B-cell lymphoma-2 (bcl-2) in a dose- and time-dependent manner. In conclu­sion, this is the first report demonstrating the anticancer and pro-apop­tosis effects of DHM on AGS human gastric cancer cells. The results strongly suggest that DHM may be a potential therapeutic candidate for the treatment of gastric cancer.