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Background <p>Bladder cancer (BCa) is one of the most common types of cancers prevalent in the global populace, and it is predominantly detected among men. The role of carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) in promoting invasion and metastasis in cancers is well known. Despite this, the precise regulatory mechanism by which CEACAM6 contributes to BCa progression remain poorly understood, which is precisely the focus of the present study.</p> Methods <p>Our research generated BCa cell lines with CEACAM6 overexpression/knockdown to evaluate the functional significance of CEACAM6. We assessed how the modulation of CEACAM6 influences cell proliferation both in vitro and in vivo on BCa progression. In addition, the effect of CEACAM6 on glycolytic activity was also explored. The co-localization, co-immunoprecipitation, ubiquitination studies, and rescue experiments were performed to understand the molecular interaction between CEACAM6 and alpha-Enolase 1 (ENO1).</p> Results <p>Our data show that high CEACAM6 expression promotes proliferation, invasion, migration, and clonogenicity of BCa cells. Additionally, CEACAM6 binding to ENO1 and maintain its stability, leading to increased glycolytic activity and invasiveness and proliferative of BCa cells.</p> Conclusion <p>Our study demonstrated that CEACAM6 regulates glycolysis via the ENO1-AKT/mTOR axis. These results offer new evidence about previously unexplored molecular mechanisms driving BCa progression.</p>

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CEACAM6 regulates glycolytic metabolism in bladder cancer cell by controlling ENO1 stability

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月11日

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  • Pu Wang,
  • Changchang Li,
  • Yangyang Xu,
  • Saleh Altuwaijri,
  • Yuanjie Niu,
  • Yang Zhao,
  • Ning Jiang

摘要

Background

Bladder cancer (BCa) is one of the most common types of cancers prevalent in the global populace, and it is predominantly detected among men. The role of carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) in promoting invasion and metastasis in cancers is well known. Despite this, the precise regulatory mechanism by which CEACAM6 contributes to BCa progression remain poorly understood, which is precisely the focus of the present study.

Methods

Our research generated BCa cell lines with CEACAM6 overexpression/knockdown to evaluate the functional significance of CEACAM6. We assessed how the modulation of CEACAM6 influences cell proliferation both in vitro and in vivo on BCa progression. In addition, the effect of CEACAM6 on glycolytic activity was also explored. The co-localization, co-immunoprecipitation, ubiquitination studies, and rescue experiments were performed to understand the molecular interaction between CEACAM6 and alpha-Enolase 1 (ENO1).

Results

Our data show that high CEACAM6 expression promotes proliferation, invasion, migration, and clonogenicity of BCa cells. Additionally, CEACAM6 binding to ENO1 and maintain its stability, leading to increased glycolytic activity and invasiveness and proliferative of BCa cells.

Conclusion

Our study demonstrated that CEACAM6 regulates glycolysis via the ENO1-AKT/mTOR axis. These results offer new evidence about previously unexplored molecular mechanisms driving BCa progression.