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Background <p>Bladder cancer (BLCA) is the second most common genitourinary malignancy worldwide, and its prognosis is poor. Carboxypeptidase E (CPE) enzyme plays a vital role in regulating biosynthesis and has been associated with cancer. However, the prognostic roles of CPE in bladder cancer have not been documented so far.</p> Methods <p>The expression status, potential molecular mechanism, and prognostic value of CPE in BLCA were investigated using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. In addition, its biological roles in BLCA were explored through in vitro studies.</p> Results <p>By analyzing data from the TCGA and the GEO databases, we discovered that patients with a high level of CPE had a worse overall prognosis from TCGA BLCA cohort. Furthermore, CPE was identified as an independent risk factor for survival of BLCA patients. These findings suggest a potential association between CPE expression and prognosis of BLCA patients. The underlying biological mechanism may involve CPE’s influence on epithelial–mesenchymal transition (EMT) and the tumor microenvironment (TME). An in vitro study revealed that CPE knockdown inhibited BLCA cell proliferation and growth.</p> Conclusions <p>Our multi-omics and functional assays link high CPE expression to poorer survival and signatures of EMT and immune exhaustion in bladder cancer, positioning CPE as a candidate prognostic marker for prospective validation.</p>

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High carboxypeptidase E expression correlates with poor bladder cancer survival: retrospective multi-omics and in vitro analysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月20日

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  • Wenping Guo,
  • Rui Cao,
  • Wenwen Wang,
  • Jishi Lv,
  • Yuxing Xie,
  • Zhuoyi Zhang,
  • Wang Quan

摘要

Background

Bladder cancer (BLCA) is the second most common genitourinary malignancy worldwide, and its prognosis is poor. Carboxypeptidase E (CPE) enzyme plays a vital role in regulating biosynthesis and has been associated with cancer. However, the prognostic roles of CPE in bladder cancer have not been documented so far.

Methods

The expression status, potential molecular mechanism, and prognostic value of CPE in BLCA were investigated using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. In addition, its biological roles in BLCA were explored through in vitro studies.

Results

By analyzing data from the TCGA and the GEO databases, we discovered that patients with a high level of CPE had a worse overall prognosis from TCGA BLCA cohort. Furthermore, CPE was identified as an independent risk factor for survival of BLCA patients. These findings suggest a potential association between CPE expression and prognosis of BLCA patients. The underlying biological mechanism may involve CPE’s influence on epithelial–mesenchymal transition (EMT) and the tumor microenvironment (TME). An in vitro study revealed that CPE knockdown inhibited BLCA cell proliferation and growth.

Conclusions

Our multi-omics and functional assays link high CPE expression to poorer survival and signatures of EMT and immune exhaustion in bladder cancer, positioning CPE as a candidate prognostic marker for prospective validation.