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The present study aimed to examine the roles and mechanisms of metformin in the stemness and epithelial‑mesenchymal transition (EMT) of colorectal cancer cells. The formation of spheroid cells, and the results of reverse transcription‑quantitative polymerase chain reaction and western blot analyses showed that metformin suppressed the ability to form spheroid cells and the expression of stemness markers in HCT116 colorectal cancer cells. Additionally, metformin attenuated the EMT process, characterized by a decrease of mesenchymal marker Vimentin and an increase in the expression of an epithelial marker. Mechanistically, metformin inactivated the Wnt3a/β‑catenin signaling pathway, and reactivation of Wnt3a/β‑catenin signaling attenuated the inhibition of metformin on the stemness of HCT116 colorectal cancer cells and EMT. Finally, it was revealed that metformin re‑sensitized HCT116 sphere cells to 5‑fluorouracil resistance. These results suggest that metformin can attenuate stemness and EMT in colorectal cancer cells.

Metformin attenuates cells stemness and epithelial‑mesenchymal transition in colorectal cancer cells by inhibiting the Wnt3a/β‑catenin pathway