MiR-623 links lncRNA RP11-89 and cyclin D1 to regulate the proliferation of glioblastoma cells

Abstract

Purpose The tumorigenesis of bladder cancer has been proven to be related to the increased expression of lncRNA RP11-89, the participation of which in glioblastoma (GBM) is unknown. We predicted that RP11-89 could be targeted by miR-623, which targets cyclin D1. We then analyzed the role of RP11-89 in GBM. Materials and methods Samples of both GBM and paired non-tumor tissue were obtained from 58 GBM patients to analyze the expression of RP11-89 and miR-623 through RT-qPCR. The direct binding of miR-623 to RP11-89 was analyzed with RNA-RNA pull down. The role of RP11-89 and miR-623 in regulating each other’s expression was analyzed with overexpression assay. The role of RP11-89 and miR-623 in regulating the expression of cyclin D1 and GBM cell proliferation was analyzed by Western blot and BrdU assay, respectively. Results RP11-89 was expressed in high amounts in GBM, while miR-623 was expressed in low amounts in GBM. RP11-89 and miR-623 were not closely correlated, while miR-623 directly bound to RP11-89. RP11-89 and miR-623 showed no direct role in each other’s expression. RP11-89 suppressed the role of miR-623 in downregulating cyclin D1 and GBM cell proliferation. Conclusions Therefore, miR-623 may link lncRNA RP11-89 and cyclin D1 to regulate the proliferation of GBM cells.