Abstract
Glioblastoma is the most common primary malignancy of the adult central nervous system and is associated with a markedly poor prognosis. Elucidating the pathogenesis and molecular changes will assist in further understanding the pathogenesis and progression of the disease and offer novel targets for therapies. The present study demonstrated that the expression level of GK5 was lower in high-grade glioblastoma tissues compared with low-grade ones and it can promote proliferation in glioblastoma cells. The regulatory mechanism of GK5 in glioblastoma were also investigated. It was revealed that GK5 is a target of miR-135b in U87MG glioblastoma cells. Controry to GK5, the expression of miR-135b is upregulated in glioblastoma and its expression is positively associated with the grade of the disease. Finally, it was demonstrated that miR-135b promoted the proliferation of U87MG cells. Therefore, miR-135b may function as an oncogene by inhibiting GK5 in glioblastoma.