MiR-361-5p inhibits cell proliferation and induces cell apoptosis in retinoblastoma by negatively regulating CLDN8.

Abstract

MiR-361-5p has been reported to act as tumor suppressor in several types of cancers. Retinoblastoma (RB) is the most common ocular tumor in childhood. The current study aimed to investigate the expression pattern and biological function of miR-361-5p in RB. Quantitative real time was utilized to determine and compare the expression of miR-361-5p in RB cells and normal retinal pigment epithelial cell line ARPE-19. CCK-8 and Edu assay were performed to assess cell proliferation. Cell apoptosis was evaluated using flow cytometry assay. Bioinformatics databases and luciferase reporter assay were applied to predict and confirm the target gene of miR-361-5p in RB cells. Here, we found miR-361-5p was significantly downregulated in RB cells compared with normal retinal pigment epithelial cell line ARPE-19. MiR-361-5p overexpression significantly inhibited or silencing promoted cell proliferation in Y79 and SO-RB50 cells, respectively. Flow cytometry assay showed a significantly decreased cell apoptosis in miR-361-5p silencing Y79 cells and increased cell apoptosis in miR-361-5p overexpressing SO-RB50 cells. Moreover, miR-361-5p directly bound to the 3' untranslated region of claudin 8 (CLDN8) and inhibited the expression of CLDN8. Furthermore, we found knockdown of CLDN8 photocopied the effect of miR-361-5p on cell proliferation and apoptosis in RB cells. These results indicated that overexpression of miR-361-5p might act as a suppressor in RB by targeting CLDN8 to inhibit the cellular function.