| BACKGROUND: Bladder cancer is one of the most common malignant tumours encountered in urology in China,but its pathogenesis remains obscure.Some studies have shown that DNA damage repair is highly correlated with tumour development and drug resistance,etc.Through bioinformatics analysis,we found that the homologous recombination repair gene RAD54 L plays an important role in the development of bladder cancer,etc.However,its mechanism of effect is not yet clear.METHODS: The differential genes expressed in the bladder cancer gene matrix were analysed,and the differential genes were subject to core gene screening,followed by protein interaction analysis and gene function enrichment analysis.The effects of RAD54 L on bladder cancer cells were verified by cell clone formation assay,Celigo cell counting assay and MTT assay;PI-FACS to explore cell cycle;SA-b-gal staining to detect bladder cancer cell senescence;Western blotting to examine cell cycle and cell senescence-related protein expression.The effect of RAD54 L on bladder cancer cells in vivo was verified by tumour formation in nude mice;the relationship between RAD54 L and prognosis of bladder cancer patients was analysed by immunohistochemistry.RESULTS: Bioinformatics analysis revealed that RAD54 L plays an important role in the development of bladder cancer by participating in nuclear division,DNA damage repair and cell cycle processes.In vitro cellular assays revealed that RAD54 L could promote bladder cancer cell proliferation,inhibit bladder cancer apoptosis,promote cell cycle progression and inhibit cellular senescence.In vivo animal experiments confirmed that RAD54 L could promote bladder cancer cell proliferation in animals.Immunohistochemical analysis revealed that high RAD54 L expression was associated with poor prognosis in bladder cancer patients.CONCLUSION: RAD54 L may promote bladder cancer cell proliferation by promoting bladder cancer cell cycle progression and inhibiting cellular senescence. |
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