Objective To investigate the role of RAD51 in cell proliferation, migration and chemosensitivity to temozolomide (TMZ) using U251 glioma cell line, and to clarify the underlying molecular mechanism. Methods TCGA database was utilized to analyze the expression changes of RAD51 in gliomas. RAD51 was over-expressed or knocked down in U251 glioma cells via lentivirus infection, or its activity was inhibited by small molecule inhibitors. Cell proliferation and migration ability were examined by CCK-8 assay, colony formation assay, and scratch wound-healing assay; CCK-8 assay and flow cytometry were performed to assess the effect of RAD51 on the sensitivity of glioma cells upon the treatment of temozolomide. Western blotting was used to determine the alteration of P53. Results The expression of RAD51 significantly increased in glioma tissues. RAD51 enhanced the proliferation and migration ability of U251 glioma cells; knockdown of RAD51 enhanced the sensitivity of U251 glioma cells to temozolomide. Over-expression of RAD51 increased the expression of P53, whereas knockdown of RAD51 decreased the expression of P53. Conclusion RAD51 plays an oncogene function in glioma cells. RAD51 over-expression enhances the proliferation and migration of glioma cells. RAD51 knockdown increases the sensitivity of glioma cells to temozolomide.
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