CDCA5 promotes the progression of prostate cancer by affecting the ERK signalling pathway

Cell division cycle-associated 5 (CDCA5) can regulate cell cycle-related proteins to promote the proliferation of cancer cells. The purpose of the present study was to investigate the expression level of CDCA5 in prostate cancer (PCa) and its effect on PCa progression. The signalling pathway by which CDCA5 functions through was also attempted to elucidate. Clinical specimens of PCa patients were collected from the Second Hospital of Tianjin Medical University. The expression level of CDCA5 in cancer tissues and paracancerous tissues from PCa patients was detected by RT-qPCR analysis and IHC. The relationship between the expression level of CDCA5 and the survival rate of PCa patients was analysed using TCGA database. Two stable cell lines (C4-2 and PC-3) with CDCA5 knockdown were established, and the effects of CDCA5 on PCa cell proliferation were detected by MTT and colony formation assays. Flow cytometry was performed to detect the effect of CDCA5 on the PCa cell division cycle, and western blot analysis was used to determine changes in ERK phosphorylation levels after CDCA5 knockdown. The effect of CDCA5 expression on prostate tumour growth was assessed using a mouse xenograft model. The results revealed that the mRNA and protein expression levels of CDCA5 were significantly higher in PCa tissues than in paracancerous tissues. High CDCA5 expression was associated with the prognosis of patients with PCa. CDCA5 expression knockdown significantly reduced the number of PCa cells in mitoses and inhibited their proliferation in vitro and in vivo. When CDCA5 was knocked down, the phosphorylation level of ERK was also reduced. Collectively, CDCA5 was upregulated and affected the prognosis of patients with PCa. Decreased CDCA5 expression inhibited PCa cell proliferation by inhibiting the ERK signalling pathway. Thus, CDCA5 may be a potential therapeutic target for PCa.