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

• Published in: Genetics and molecular research Vol. 14; no. 4; pp. 15564 - 15571
• Main Authors: Ji, F J, Tian, X F, Liu, X W, Fu, L B, Wu, Y Y, Fang, X D, Jin, H Y
• Format: Journal Article
• Language: English
• Published: Brazil 01.01.2015
• Subjects: Antineoplastic Agents, Phytogenic - pharmacology; Apoptosis - drug effects; Apoptosis - genetics; Apoptosis Regulatory Proteins - genetics; Cell Line, Tumor; Cell Proliferation - drug effects; Cell Survival - drug effects; Flavonols - pharmacology; Gene Expression Regulation, Neoplastic - drug effects; Humans; Signal Transduction - drug effects; Stomach Neoplasms - genetics; Stomach Neoplasms - metabolism; Tumor Suppressor Protein p53 - metabolism
• ISSN: 1676-5680; 1676-5680
• DOI: 10.4238/2015.December.1.7

The aim of the present study was to determine the anti-proliferative 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-di-methylthiazol-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.