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Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
ISSN: 1596-5996
EISSN: 1596-9827
Vol. 15, No. 11, 2016, pp. 2365-2370
Bioline Code: pr16312
Full paper language: English
Document type: Research Article
Document available free of charge

Tropical Journal of Pharmaceutical Research, Vol. 15, No. 11, 2016, pp. 2365-2370

 en Apigenin inhibits proliferation and migratory properties of Barrett's esophageal adenocarcinoma cells by targeting PI3K/Akt/mTOR pathway
Wang, Zhan & Zheng, Peng-yuan


Purpose: To investigate the effect of apigenin on Barrett's esophagus–associated esophageal adenocarcinoma (BEAC) cells OE33, and also to ascertain the mechanism by which it inhibits cellular proliferation and motility.
Methods: Proliferation index of OE33 in the absence and presence of apigenin was determined by methyl-thiazolyl-tetrazolium (MTT) assay and apoptosis was determined by enzyme-linked immunosorbent assay (ELISA) method. Boyden Chamber’s assay was applied to determine the migration and invasion of control and apigenin-treated OE33 cells. Status of PI3K/Akt/mTor signaling was further determined by Western blotting in control and apigenin-treated cells.
Results: Apigenin resulted in the inhibition of the proliferation of OE33 cells in a dose- and time-dependent fashion, with an IC50 of 75 μM, after 72 h of incubation, and also induced apoptosis, with modulation of pro- and anti-apoptotic genes. Furthermore, apigenin inhibited the motility of OE33 by targeting PI3K/Akt/mTOR signaling.
Conclusion: Apigenin effectively inhibits the oncogenicity of OE33 cells by targeting PI3K/Akt/mTOR pathway.

Barrett's esophagus–associated esophageal adenocarcinoma (BEAC); Apoptosis; Migration; Anticancer

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