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The effects of Curcumin on HCT‐116 cells proliferation and apoptosis via the miR‐491/PEG10 pathway

Paternally expressed gene‐10 (PEG10) could participate in several carcinomas and might be regulated by miR‐491. To now, miR‐491 was found to play an important role in the sensitivity and mechanism of drug usage in the treatment of colorectal cancer, and drug resistance is a key factor to affect the disease healing. In this study, miR‐491, PEG10, Wnt1, and β‐catenin expression levels and their correlation with colorectal cancer were assessed in cancer tissues and adjacent parts. And the target relationship between PEG10 and miR‐491 was verified. Meanwhile, the impaction of Curcumin on miR‐491, PEG10, and Wnt/β‐catenin signaling pathway were analyzed in HCT‐116 cells. The effects of PEG10 and Curcumin on human HCT‐116 cells proliferation and apoptosis were investigated by MTT and flow cytometry assay. Results showed that the expression of miR‐491 in colon cancer tissues was decreased, but PEG10, Wnt1, and β‐catenin were higher than that in adjacent tissues. The PEG10 gene 3′ UTR could combine with miR‐491 seed sequence and miR‐491 overexpression could cause a decrease in PEG10, Wnt1, and β‐catenin levels in human HCT‐116 cells. Furthermore, PEG10 overexpression increased the expression levels of Wnt1 and β‐catenin, thereby promoting cell proliferation and inhibiting apoptosis. In addition, Curcumin could up‐regulate miR‐491, inhibit PEG10, and Wnt/β‐catenin signaling pathway. Consequently, Curcumin reduced HCT‐116 cells proliferation and promoted cells apoptosis via the miR‐491/PEG10 pathway. In conclusion, PEG10 was a target gene of miR‐491, miR‐491/PEG10 strengthen the sensitivity of Curcumin in HCT‐116 cells proliferation and apoptosis, which might act as an ideal diagnostic biomarker treatment methods.