The lncRNA MIR22HG suppresses prostate cancer cell proliferation, migration, and epithelial-mesenchymal transition via the miR-4428/PCDH9 axis.

Background: Long non-coding RNAs (lncRNAs) play crucial roles in modulating the development and progression of human malignant cancers. As a tumour suppressor gene, the lncRNA MIR22HG has been identified in many kinds of cancers. However, the specific function of MIR22HG in prostate cancer (Pca) has yet to be elucidated. Specifically, we sought to determine whether MIR22HG plays a role in Pca progression and the underlying mechanisms involved.

Methods: Differentially expressed lncRNAs in Pca tissues were screened by sequencing, and the expression of MIR22HG in cells and tissues was determined via quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK8), Transwell, and western blotting assays were used to determine whether Pca cell proliferation and migration can be regulated by the MIR22HG/microRNA-4428 (miR-4428)/PCDH9 axis. To investigate tumour growth in vivo, we constructed tumour subcutaneous xenograft models. Moreover, we performed bioinformatic analysis and dual-luciferase reporter assays to verify the expression of the miR-4428 and PCDH9 targets.

Results: MIR22HG was expressed at low levels in Pca cells and tissues, and its upregulation inhibited cell proliferation and migration and prevented epithelial-mesenchymal transition (EMT) in vivo and in vitro. A negative correlation was found between MIR22HG expression and miR-4428 expression. The downstream target gene of miR-4428 was PCDH9. Therefore, MIR22HG may function as a competing endogenous RNA (ceRNA) to regulate miR-4428/PCDH9.

Conclusions: We demonstrated that MIR22HG acts as a tumour suppressor in Pca and suggested that targeting the MIR22HG/miR-4428/PCDH9 axis may be a new avenue for Pca therapy.