Open Access

ARTICLE

Ectopic Expression of miR-147 Inhibits Stem Cell Marker and Epithelial–Mesenchymal Transition (EMT)-Related Protein Expression in Colon Cancer Cells

Xiaofei Ning^*, Cong Wang^†, Meng Zhang^†, Kecheng Wang^*

* Department of Gastrointestinal Surgery, Affiliated Hospital of Jining Medical College, Jining, P.R. China
† Department of Medical Ultrasonography, Affiliated Hospital of Jining Medical College, Jining, P.R. China

Oncology Research 2019, 27(4), 399-406. https://doi.org/10.3727/096504018X15179675206495

Abstract

Colon cancer is one of the most common cancers in the world. Epithelial-to-mesenchymal transition (EMT) is a crucial step in tumor progression and is also involved in the acquisition of stem cell-like properties. Some miRNAs have been shown to function as either tumor suppressors or oncogenes in colon cancer. Here we investigated the role of miR-147 in the regulation of the stem cell-like traits of colon cancer cells. We observed that miR-147 was downregulated in several colon cancer cell lines, and overexpressed miR-147 decreased the expression of cancer stem cell (CSC) markers OCT4, SOX2, and NANOG in the colon cancer cell lines HCT116 and SW480. Overexpressed miR-147 inhibited EMT by increasing the expression of epithelial markers E-cadherin and -catenin while decreasing the expression of mesenchymal markers fibronectin and vimentin. Moreover, activation of EMT by TGF- 1 treatment significantly counteracted the inhibitive effect of miR-147 on the expression of CSC markers OCT4, SOX2, and NANOG, supporting the idea that overexpressing miR-147 inhibited stem cell-like traits by suppressing EMT in colon cancer. In addition, we found that overexpressed miR-147 downregulated the expression of -catenin, c-myc, and survivin, which were related to the Wnt/ -catenin pathway. Moreover, treatment of miR-147 mimic-transfected cells with the Wnt/ -catenin pathway activator LiCl attenuated the inhibitive effect of the miR-147 mimic on the EMT and stem cell-like traits of colon cancer cells, indicating that ectopic expression of miR-147 inhibited stem cell-like traits in colon cancer cells by suppressing EMT via the Wnt/ -catenin pathway. In summary, our present study highlighted the crucial role of miR-147 in the inhibition of the stem cell-like traits of colon cancer cells and indicated that miR-147 could be a promising therapeutic target for colon cancer treatment.

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