miR-497/MIR497HG inhibits glioma cell proliferation by targeting CCNE1 and the miR-588/TUSC1 axis

Emerging evidence has shown that microRNA (miR)-497 serves pivotal roles in tumorigenesis, cancer progression, metastasis and chemotherapy resistance in several types of cancer. In the present study, the expression and biological functions of miR-497 host gene (MIR497HG) were investigated in glioma tissue. The expression levels of miR-497 and MIR497HG were measured in glioma, adjacent non-cancerous and normal brain tissue and their association with the prognosis of patients with glioma were analyzed. The biological roles of miR-497 and MIR497HG were investigated in glioma cell lines. In addition, bioinformatics analysis, luciferase reporter assay and functional experiments were performed to identify and validate the downstream targets of miR-497 or MIR497HG. The expression levels of miR-497 and MIR497HG were downregulated in glioma tissue and cell lines compared with those in adjacent non-cancerous and normal brain tissue and normal human cortical neuron cell line. Patients with low miR-497 or MIR497HG expression levels exhibited a poor prognostic outcome. In addition, forced overexpression of miR-497 or MIR497HG significantly inhibited the proliferation and cell cycle progression of glioma cell lines. Furthermore, the results indicated that miR-497 and MIR497HG exerted their biological functions by direct targeting of cyclin E1 and miR-588/tumor suppressor candidate 1. In summary, the data indicated that miR-497 and MIR497HG served as tumor suppressors and may be used as potential therapeutic targets and prognostic biomarkers in glioma.

Automated summary

MicroRNA (miR)-497 and its host gene MIR497HG play important roles in tumorigenesis, cancer progression, and chemotherapy resistance in glioma. Low expression levels of miR-497 or MIR497HG are associated with poor prognosis in glioma patients, while overexpression inhibits proliferation and cell cycle progression of glioma cells. They function by directly targeting cyclin E1 and miR-588/tumor suppressor candidate 1.