MIR22HG Regulates the Proliferation, Epithelial-Mesenchymal Transition, and Apoptosis in Colorectal Carcinoma.

Background

Recent investigations have suggested that long noncoding RNA (lncRNA) MIR22HG is commonly dysregulated in multiple types of malignancies. Nevertheless, the role of these MIR22HG in human colorectal carcinoma (CRC) are not well explored. Materials and

Methods

Quantitative real-time polymerase chain reaction (qPCR) and in situ hybridization (ISH) assay were used to measure the expression of MIR22HG. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and migration, as well as invasion assays, were utilized to determine the roles of MIR22HG on growth, apoptosis, migration, and invasiveness of CRC cell. The expression of E-cadherin and N-cadherin was measured using Western blotting and immunohistochemistry staining assay. CRC cell growth in vivo was analyzed using nude mice xenograft.

Results

The qPCR and ISH assay revealed that MIR22HG was downregulated in CRC sample compared with in normal tissue. MIR22HG was also significantly downexpressed in CRC cells compared with that in normal colonic epithelial cell line. Overexpression of MIR22HG inhibited the growth, migration ability, and invasiveness of CRC cell in vitro. In addition, MIR22HG suppressed the epithelial-mesenchymal transition (EMT) and induced the apoptosis of human CRC cell. Moreover, the authors demonstrated that MIR22HG inhibited the tumor growth of CRC cell and regulated the expression of EMT markers (E-cadherin and N-cadherin) in vivo.

Conclusion

Altogether, these results imply that lncRNA MIR22HG restrained the aggressive phenotypes of CRC cell.