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colon cancer; 2α,3α,24-trihydroxy-12-alkene-28-ursolic acid; proliferation; invasion; migration; apoptosis
Aim: We aimed to evaluate the effects of 2α,3α,24-trihydroxy-12-alkene-28-ursolic acid (TEOA) on the proliferation, invasion, migration and apoptosis of human colon cancer cell line HCT116 as well as the mechanism. Methods: HCT116 cells were treated with different concentrations of TEOA (0 μM, 20 μM, 40 μM, 60 μM). The cell proliferation was detected by MTT and colony formation assays. The migration and invasion were tested by Transwell assay, and the apoptosis was studied by flow cytometry. Autophagic vacuoles were observed by fluorescence microscopy. The protein expressions of apoptosis markers caspase-9 and PARP as well as autophagy markers LC3-II and p62 were detected by Western blot. Results: TEOA had growth inhibitory effects on HCT116 cells in time- and dose-dependent manners. The cell proliferation was significantly inhibited after TEOA treatment, and the size and number of colonies were significantly lower than those of control cells. After TEOA treatment, the invasion and migration abilities of HCT116 cells decreased significantly. TEOA caused apoptosis of HCT116 cells dose-dependently. After 48 h of treatment, TEOA activated the protein expressions of caspase-9, PARP, LC3-II and p62, which also increased with rising dose. Conclusion: TEOA can significantly inhibit the proliferation, invasion and migration of human colon cancer HCT116 cells, and promote their apoptosis, probably being related to autophagy.
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