LncRNA MIR7-3HG executes a positive role in retinoblastoma progression via modulating miR-27a-3p/PEG10 axis.

Homo sapiens MIR7-3 host gene (MIR7-3HG), a long non-coding RNA, has been reported to be connected with the progression of several tumors and could be served as a prognostic marker. Our study intends to explore the biological function and potential molecular mechanism of MIR7-3HG in Retinoblastoma (Rb) progression. Two Rb cell lines Y79 and WERI-Rb-1 were applied to perform functional assays. Expression of MIR7-3HG in Rb tissues and cells were determined with the support of GEO database and qRT-PCR experiment. The effects of MIR7-3HG on cell activity and apoptosis were assessed through cell counting kit 8 and flow cytometry assays, respectively. Targeted connections between MIR7-3HG and miR-27a-3p, as well as miR-27a-3p and PEG10 were speculated by bioinformatics prediction software and verified by performing dual luciferase assays. Further interrelationships among MIR7-3HG, miR-27a-3p, and PEG10 were explored through rescue assays. MIR7-3HG overexpression was detected in Rb tissues and cell lines. Depletion of MIR7-3HG reduced the activity of Rb cells and increased the apoptosis of Rb cells, and vice versa. In addition, further exploration perceived that MIR7-3HG, miR-27a-3p, and PEG10 generated a competing endogenous RNA (ceRNA) mechanism to regulate Rb cells activity and apoptosis. Our results indicated that MIR7-3HG functioned as a ceRNA to up-regulate PEG10 expression via sponging miR-27a-3p to promote the proliferation of Rb cells and suppress the apoptosis of Rb cells, exhibiting a group of potential target molecules for Rb treatment in the future.