miR-548a-3p Weakens the Tumorigenesis of Colon Cancer Through Targeting TPX2

Background: MicroRNA (miRNA) has been verified as the significant factor to participate in the progression of colon cancer (CC). In this study, the authors are committed to investigate the mechanism and function of miR-548a-3p in CC. Methods: Bioinformatics analysis was used to analyze the mRNA expression profile and miRNA expression profile from GEO data series. The expression of miRNA and mRNA was analyzed by real-time quantification polymerase chain reaction in 43 pairs of CC clinical tissue samples and CC cells. The western blot assay was used to detect the TPX2 protein. Then, SW480 and HCT116 cells were stably transfected with miR-548a-3p mimic, miR-548a-3p inhibitor, TPX2 overexpression, and TPX2 siRNA constructs to study the effects of miR-548a-3p and TPX2. Cellular functional experiments included cell counting kit-8 assay, BrdU incorporation assay, and wound healing assay. In addition, luciferase reporter assay was applied to detect the regulatory association between miR-548a-3p and TPX2. Results: TPX2 and miR-548a-3p were identified as the interested mRNA and miRNA by microarray analysis. In CC tissues and cell lines, miR-548a-3p with low expression and TPX2 with high expression were observed. What's more, exogenous overexpressed miR-548a-3p impaired the cell viability, cell proliferation, and cell migration, while TPX2 overexpression enhanced the malignancy phenotypes. However, the promotion effect of TPX2 on CC cells was impaired by miR-548a-3p. Conclusion: This study revealed that miR-548a-3p attenuated the development of CC by targeting TPX2.

Automated summary

This study revealed that miR-548a-3p attenuated the development of colon cancer by targeting TPX2. Low expression of miR-548a-3p and high expression of TPX2 were observed in colon cancer tissues and cell lines. Overexpression of miR-548a-3p inhibited cell viability, proliferation, and migration, while TPX2 overexpression enhanced the malignancy phenotypes of colon cancer.