Apigenin inhibits proliferation and migratory properties of Barrett's esophageal adenocarcinoma cells by targeting PI3K/Akt/mTOR pathway
Abstract
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 timedependent 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.
Keywords: Barrett's esophagus–associated esophageal adenocarcinoma (BEAC), Apoptosis, Migration, Anticancer
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