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<p>Bladder cancer (BC) is characterized by a high incidence and frequent recurrence. Despite efforts to improve survival and reduce mortality among BC patients, significant progress remains elusive. The role of the cell cycle in BC has been increasingly studied, and our analysis revealed that BC exhibits elevated expression of BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B). However, the role of BUB1B in BC remains not fully understood. A Multi-omics analysis was performed by integrating BUB1B expression with clinical data, and the results indicated that the upregulation of BUB1B was associated with poor prognosis. Moreover, our study demonstrated that BUB1B promotes bladder cancer (BC) cell proliferation, migration, invasion, and tumorigenicity both in vitro and in vivo. Finally, subsequent analysis revealed a positive correlation of BUB1B expression with CDC25A and IFI6, and a negative correlation with CXCR6 and RGS4. In addition, our findings implicate​ the NF-κB signaling pathway in the function of BUB1B. These findings provided insights into the potential role of BUB1B as a therapeutic target for BC.</p>

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Multi-omics analysis identifies BUB1B as a cell cycle–related driver of bladder cancer progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月12日

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  • Huidong Zhou,
  • Shao Peng,
  • Zhixin Ling,
  • Jiaodi Cai,
  • Jinghong Liu,
  • Ying Kong,
  • Hua Zhang,
  • Jun Ouyang,
  • Jianglei Zhang

摘要

Bladder cancer (BC) is characterized by a high incidence and frequent recurrence. Despite efforts to improve survival and reduce mortality among BC patients, significant progress remains elusive. The role of the cell cycle in BC has been increasingly studied, and our analysis revealed that BC exhibits elevated expression of BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B). However, the role of BUB1B in BC remains not fully understood. A Multi-omics analysis was performed by integrating BUB1B expression with clinical data, and the results indicated that the upregulation of BUB1B was associated with poor prognosis. Moreover, our study demonstrated that BUB1B promotes bladder cancer (BC) cell proliferation, migration, invasion, and tumorigenicity both in vitro and in vivo. Finally, subsequent analysis revealed a positive correlation of BUB1B expression with CDC25A and IFI6, and a negative correlation with CXCR6 and RGS4. In addition, our findings implicate​ the NF-κB signaling pathway in the function of BUB1B. These findings provided insights into the potential role of BUB1B as a therapeutic target for BC.