Abstract
Glioma is a common primary intracranial brain disease that exhibits an increasing incidence and mortality rate. Accumulating evidences have suggested that Ribosomal protein S14 (RPS14) was involved in cell proliferation and tumor progression. Nevertheless, the biological function and underlying mechanism of RPS14 in glioma are still largely unclear. Herein, we found that RPS14 was overexpressed in glioma. In the loss-of-function experiments, RPS14 depletion markedly suppressed glioma cell proliferation, migration and prompted cell apoptosis in vitro. Further study suggested that RPS14 depletion inhibited tumor growth of glioma in vivo. Additionally, human phospho-kinase array profiling and Western blot analysis revealed that the effects of RPS14 knockdown on glioma may be closely associated with p53 signaling pathway. Further study indicated that addition of p53 inhibitor pifithrin-α (PFT-α) could attenuate the influences of RPS14 knockdown on cell proliferation and apoptosis. Taken together, our findings suggested that RPS14 exhibits a pro-oncogenic role in glioma progression and may be act as a novel potential therapeutic target for gliomas.