MiR-26b suppresses cell proliferation and invasion by targeting cyclooxygenase 2 in human glioblastoma

Abstract

MiRNAs are emerging as important epigenetic modulators of multiple target genes, leading to abnormal cellular signaling involving cellular proliferation in cancers. Aberrant miRNA expression has been observed in human glioblastoma (GBM). The present study was to evaluate the expression and molecular mechanisms of COX-2 and miR-26b in human GBM tissues and GBM cell lines T98G, U87 and U251. In the present study, we found that expression of miR-26b was markedly downregulated in GBM cell lines and human GBM tissues, compared to matched non-tumor associated tissues. Furthermore, miR-26b expression was inversely proportional to that of COX-2 mRNA and protein. Ectopic expression of miR-26b dramatically reduced the proliferation, colony formation, and proliferation/apoptosis-related proteins in GBM cells. Flow cytometry analysis showed that ectopic expression of miR-26b significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Finally, luciferase reporter assay revealed that miR-26b inhibited the expression of COX-2 by binding to the 3'-UTR of COX-2 in GBM cells. Taken together, our results suggest that miR-26b plays an important role to inhibit the proliferation and invasion of GBM cells, and presents a novel mechanism for direct miR-26bmediated suppression of COX-2 in GBM. Thus, miR-26b/COX-2 may have an important role in treatment of GBM patients.

microRNA-142-3p inhibits apoptosis and inflammation induced by bleomycin through down-regulation of Cox-2 in MLE-12 cells

“…It has been reported as a pivotal factor in multiple physiological functions and pathological processes, including inflammation and tumorigenesis ( 10 ). Previous studies have shown that Cox-2 has a negative correlation with the expression of several miRNAs, such as miR-26b ( 11 ), miR-203 ( 12 ), and miR-335 ( 13 ).…”