KLF5-mediated CDCA5 expression promotes tumor development and progression of epithelial ovarian carcinoma

Cell division cycle associated 5 (CDCA5) is correlated with the development and progression of many malignant tumors. However, little is known about its role in epithelial ovarian cancer (EOC) progression. In this study, the clinical value, biological function and underlying mechanisms of CDCA5 in EOC were evaluated. CDCA5 mRNA and protein levels were substantially upregulated in EOC and had a significant positive correlation with adverse clinicopathological characteristics and a poor prognosis. CDCA5 facilitated proliferation, invasion, and metastasis and disrupted mitochondrial-mediated endogenous apoptosis by activating the cell cycle pathway and inhibiting the P53 pathway in EOC cells. Conversely, knockdown of CDCA5 expression blocked the malignant activities of EOC cells and suppressed the growth of xenograft tumors in vivo. Mechanistically, the transcription factor KLF5 bound to a specific site in the CDCA5 promoter and promoted CDCA5 expression. Moreover, KLF5 overexpression rescued the negative regulation of inhibited CDCA5 expression on EOC cell proliferation. In conclusion, our findings revealed that CDCA5 promoted tumor progression of EOC via the KLF5/CDCA5/cell cycle and P53 axes, which might provide new insights into the roles of CDCA5 in EOC.

Automated summary

The study evaluated the clinical value, biological function, and underlying mechanisms of the Cell division cycle associated 5 (CDCA5) in epithelial ovarian cancer (EOC). CDCA5 was found to be upregulated in EOC and correlated with adverse clinicopathological characteristics and poor prognosis. CDCA5 promoted proliferation, invasion, and metastasis while inhibiting apoptosis in EOC cells through the activation of the cell cycle pathway and inhibition of the P53 pathway. Knockdown of CDCA5 expression inhibited malignant activities of EOC cells and suppressed tumor growth in vivo. Mechanistically, the transcription factor KLF5 promoted CDCA5 expression by binding to the CDCA5 promoter. KLF5 overexpression rescued the negative regulation of CDCA5 expression on EOC cell proliferation.