The overexpression of miR-30a affects cell proliferation of chondrosarcoma via targeting Runx2.

MicroRNAs (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 chondrosarcoma (CS). The purpose of the present study was to evaluate the expression and molecular mechanisms of Runx2 and miR-30a in human CS tissues and CS cell lines JJ012, SW1353, and L3252. In the present study, we found that the expression of miR-30a was markedly downregulated in CS cell lines and human CS tissues, compared to matched non-tumor-associated tissues. Furthermore, miR-30a expression was inversely proportional to that of Runx2 messenger RNA (mRNA) and protein. Upregulation of miR-30a dramatically reduced the proliferation, colony formation, and cell cycle-related proteins of CS cells. Flow cytometry analysis showed that ectopic expression of miR-30a significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Luciferase reporter assays confirmed that miR-30a binding to the 3'-untranslated region (3'-UTR) region of Runx2 inhibited the expression of Runx2 in cancer cells. Taken together, our results suggest that miR-30a plays an important role to inhibit the proliferation of CS cells and presents a novel mechanism for direct miRNA-mediated suppression of Runx2 in CS. Thus, miR-30a/Runx2 may have an important role in treatment of CS patients.