MRPS 16 Regulates NFATC 2 Through the Wnt/β‐Catenin Pathway to Promote Glioma Proliferation

There have been reports that overexpression of mitochondrial ribosomal protein S16 (MRPS16) can greatly improve the growth of tumour cells, migration and invasion abilities in many ways. However, the role of MRPS16 in glioma cell proliferation, which is closely associated with tumour malignancy, remains unclear. The study applied a human gene expression array to investigate the expression levels of genes within glioma tissues in comparison with normal brain tissue. By RT‐PCR, cell counting, flow cytometry, MTT assays, colony formation and injection of mice, we deeply explored the role of MRPS16 in glioma cell growth and the underlying mechanism. MRPS16 expression was significantly higher in glioma tissues compared with normal brain tissues. In the cultured glioma cells, glioma cell proliferation was inhibited, and cell cycle arrest and cell apoptosis were induced after MRPS16 knockdown. In BALB/c mice inoculated with glioma cells knocked down for MRPS16, it was found that tumour proliferation and growth were relatively slower than the control. Through further prediction and gene transformation of cultured cells, it is confirmed that the presence of MRPS16 promotes the proliferation of glioma cells through the Wnt/β‐catenin/NFATC2 pathway. MRPS16 and NFATC2 promote glioma cell proliferation, which was confirmed by in vivo BALB/c mice inoculation. The Wnt/β—Catenin/NFATC2 pathway plays a role in promoting glioma cell proliferation by MRPS16, which is shown in our experimental data. Inhibition of MRPS16 may be a promising and effective treatment option for gliomas.