Glioblastoma has been reported as one of the leading causes of cancer-related death, and some factors including oncogenic genes and environments are involved in tumorigenesis. MicroRNAs (miRNAs) act as a kind of small and noncoding RNA, which can target the downstream molecules. Emerging reports demonstrate that microRNAs regulate the initiation and progression of different cancers. In the present study, we conducted in vitro experiment as well as clinical studies in a cohort of 20 glioblastoma samples. We demonstrated that miR-622 expression was lower in tumor tissues and cells, when compared to normal brain tissues and normal human astrocyte (NHA) cells, while K-Ras messenger RNA (mRNA) and protein showed the opposite expression profile. Overexpression of miR-622 suppressed tumor cell proliferation, migration, and invasion of A172, U87, and U251 cells. Accordingly, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 2 (MMP2), and MMP9 expressions were also decreased due to miR-622 overexpression. Importantly, we discovered that wild Kirsten rat sarcoma (K-Ras) was a direct target of miR-622, which decreased the expression of K-Ras protein in A172, U87, and U251 cells. In conclusion, upregulated miRNA-622 inhibited cell proliferation, migration, and invasion via repressing K-Ras in the progression of glioblastoma, and miR-622-K-Ras pathway can be recommended as a potential target for treatment of glioblastoma.
