LncRNA PSMB8-AS1 acts as ceRNA of miR-22-3p to regulate DDIT4 expression in glioblastoma.

Glioblastoma (GBM) is known to be one of the most fatal malignanies in central nerve system. Unfortunately, the therapies for glioblastoma still calls for further improvements. Increasing evidences have shown that the aberrant expression of long non-coding RNAs (lncRNAs) is highly relevant to glioma tumorigenesis and prognosis of GBM patients. High expression trends of lncRNA PSMB8-AS1 was observed in both glioblastoma tissues and cells. In return, GBM cell proliferation, apoptosis and radioresistance were regulated by PSMB8-AS1. In the meantime, PSMB8-AS1 mainly located in cytoplasm of glioblastoma cells, indicating post-transcriptional regulation. MiRNA-22-3p was found to contain potential binding site with PSMB8-AS1. On the other hand, low expression of miR-22-3p was exhibited in glioblastoma tissues and cells. Besides, PSMB8-AS1 and miR-22-3p had mutual suppression on the expression of each other in GBM cells. Furthermore, overexpression of PSMB8-AS1 promoted the level of DDIT4 through inhibiting miR-22-3p. Rescue assays demonstrated that overexpression of DDIT4 counteracted the impact of proliferation, apoptosis and radioresistance silencing PSMB8-AS1 lay on glioblastoma cell. Taken together, lncRNA PSMB8-AS1 acts as miR-22-3p sponge to mediate DDIT4 expression and regulate glioblastoma progression. PSMB8-AS1 might become a therapeutic target in the future.