Glioma is the most common brain tumor malignancy with high mortality and poor prognosis. Emerging evidence suggests that cancer stem cells are the key culprit in the development of cancer. MicroRNAs have been reported to be dysregulated in many cancers, while the mechanism underlying miR-150-5p in glioma progression and proportion of stem cells is unclear. The expression levels of miR-150-5p and catenin beta 1 (CTNNB1, which encodes β-catenin) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. The expression levels of downstream genes of the Wnt/β-catenin pathway and stem cell markers were detected by qRT-PCR. Tumorigenesis was investigated by cell viability, colony formation, and tumor growth in vitro and in vivo. The interaction between miR-150-5p and β-catenin was explored via bioinformatics analysis and luciferase activity assay. We found that miR-150-5p was downregulated in glioma and its overexpression inhibited cell proliferation, colony formation, and tumor growth. Moreover, miR-150-5p directly suppressed CTNNB1 and negatively regulated the abundances of downstream genes of the Wnt/β-catenin pathway and stem cell markers. Furthermore, miR-150-5p expression was decreased and β-catenin level was enhanced in CD133+ glioma stem cells. Knockdown of miR-150-5p contributed to CD133- cells with stem cell-like phenotype, whereas overexpression of miR-150-5p suppressed CD133+ glioma stem cell-like characteristics. In conclusion, miR-150-5p inhibited the progression of glioma by controlling stem cell-like characteristics via regulating the Wnt/β-catenin pathway, providing a novel target for glioma treatment.
Keywords: CTNNB1; glioma; miR-150-5p; stem cells; β-catenin.
© 2020 International Federation for Cell Biology.