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Objective: To study the effect of metformin on colon cancer HCT-116 cells through the phosphatidylinositol 3-kinase(PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling pathway. Methods: Colon cancer HCT116 cells werecultured in vitro, and metformin (20, 40, 80 μmol/L) was added to treat HCT-116 cells for 48 hours, and a control group was set up. MTTmethod was used to detect the proliferation ability of cells in each group. Transwell experiment detects the changes of cell invasion abilityin each group. The Annexin-FITC/PI double staining method was used to detect the apoptosis of each group at 48 hours after treatment. Western blotting was used to detect the protein expression level of PI3K/Akt/mTOR pathway after 48 hours. Results: Compared with thecontrol group, the metformin 20, 40, and 80 μmol/L treatment groups had a significant inhibitory effect on the proliferation of HCT-116cells, and showed concentration-dependent effect, with statistical significance (P＜0.05). Compared with the control group, the apoptoticrate of the metformin 20, 40, 80 μmol/L treatment groups were significantly higher, and showed concentration-dependent effect, with statistical significance(P＜0.05). Compared with the control group, the invasion ability of HCT116 cells in metformin 20, 40 and 80μmol/Ltreatment groups was significantly decreased, and showed concentration-dependent effect, with statistical significance (P＜0.05). Com-pared with the control group, the expression levels of Bax protein in metformin 20, 40 and 80 μmol/L treatment groups were significantlyincreased, while the expression levels of Bcl-2, p-Akt and p-mTOR protein were significantly decreased, and showed concentration-de-pendent effect, with statistical significance (P＜0.05). Conclusion: Metformin can inhibit the proliferation, apoptosis and invasion of hu-man colon cancer HCT-116 cells in vitro, and its anti-tumor mechanism may be related to the inhibition of PI3K/Akt/mTOR signalingpathway activation. [ABSTRACT FROM AUTHOR]