Journal of cancer research and clinical oncology · 2025
CDCA4 promotes bladder cancer progression by JAK/STAT signaling pathway.
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Wan Peng, Ren Yuan, Deng Hao, Li Hongtao
Аннотация
BACKGROUND: The cell division cycle associated 4 (CDCA4) plays a crucial role in various biological processes and is implicated in the progression of several tumors, however, the mechanisms by which it operates in bladder cancer remain unclear.
METHODS: Utilizing data from the TCGA and GEO datasets of bladder cancer patients, we analyzed the expression of CDCA4 and its prognostic significance. We then constructed stable overexpression and knockdown bladder cancer cell lines to investigate the effects of CDCA4 on cell proliferation, migration, and invasion in vitro, employing CCK-8, colony formation, transwell, and wound healing assays. Additionally, we validated the potential downstream pathways of CDCA4 through data analysis and western blot assays.
RESULTS: Our study found that CDCA4 expression is elevated in bladder cancer cells and correlates with poor prognosis in patients. Inhibition of CDCA4 expression reduces the proliferation, migration, and invasion of bladder cancer cells, as well as inhibit the epithelial-mesenchymal transition (EMT) process. Conversely, promoting CDCA4 expression enhances the malignancy of bladder cancer cells. Investigation into the mechanism of CDCA4 revealed that it promotes bladder cancer progression by activating the JAK/STAT signaling pathway, and the JAK inhibitor AG490 can reverse the promoting effects of CDCA4.
CONCLUSION: Our findings suggest that CDCA4 enhances the proliferation, migration, and invasion of bladder cancer cells by positively regulating the JAK/STAT signaling pathway, indicating that CDCA4 may serve as a novel molecular target for bladder cancer treatment.
METHODS: Utilizing data from the TCGA and GEO datasets of bladder cancer patients, we analyzed the expression of CDCA4 and its prognostic significance. We then constructed stable overexpression and knockdown bladder cancer cell lines to investigate the effects of CDCA4 on cell proliferation, migration, and invasion in vitro, employing CCK-8, colony formation, transwell, and wound healing assays. Additionally, we validated the potential downstream pathways of CDCA4 through data analysis and western blot assays.
RESULTS: Our study found that CDCA4 expression is elevated in bladder cancer cells and correlates with poor prognosis in patients. Inhibition of CDCA4 expression reduces the proliferation, migration, and invasion of bladder cancer cells, as well as inhibit the epithelial-mesenchymal transition (EMT) process. Conversely, promoting CDCA4 expression enhances the malignancy of bladder cancer cells. Investigation into the mechanism of CDCA4 revealed that it promotes bladder cancer progression by activating the JAK/STAT signaling pathway, and the JAK inhibitor AG490 can reverse the promoting effects of CDCA4.
CONCLUSION: Our findings suggest that CDCA4 enhances the proliferation, migration, and invasion of bladder cancer cells by positively regulating the JAK/STAT signaling pathway, indicating that CDCA4 may serve as a novel molecular target for bladder cancer treatment.