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<p>Esophageal cancer (EC) is a frequently diagnosed malignancy with limited available treatment options. Emerging evidence has underscored the significant role of tripartite motif (TRIM) proteins in various cancers. However, the specific role of TRIM11 in EC has not been elucidated. Here, we conducted a comprehensive bioinformatics analysis, along with cell line models and animal culture experiments, to investigate the role of and molecular mechanisms through which TRIM11 contributes to EC progression, and evaluate its potential as a candidate marker associated with adverse clinicopathological features. Transcriptomic analysis was conducted using data from TCGA, GTEx, CCLE, and other publicly available databases to assess TRIM11 expression and its correlation with clinicopathological features, immune infiltration and TRIM11’s relationship with treatment response in EC. In vitro experiments showed that TRIM11 overexpression significantly promoted EC cell proliferation, migration, and invasion. Flow cytometry analysis revealed that TRIM11 increased the proportion of cells entering the S phase. Mechanistically, co-immunoprecipitation assays demonstrated that endogenous TRIM11 directly interacted with Axin2 and GSK3β, two core components of the β-catenin destruction complex. Additionally, TRIM11 knockdown altered the expression of key proteins in the β-catenin signaling pathway, including CyclinD1, GSK3β, Axin2, and β-catenin. Collectively, these findings highlight TRIM11 as a pro-oncogenic factor and suggest that it is a potential functional driver of EC.</p>

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TRIM11 is upregulated in esophageal cancer and promotes tumor progression through modulation of the β-catenin signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月14日

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  • Wei Li,
  • Qingzhi Lan,
  • Shimin Lu,
  • Weiguo Dong

摘要

Esophageal cancer (EC) is a frequently diagnosed malignancy with limited available treatment options. Emerging evidence has underscored the significant role of tripartite motif (TRIM) proteins in various cancers. However, the specific role of TRIM11 in EC has not been elucidated. Here, we conducted a comprehensive bioinformatics analysis, along with cell line models and animal culture experiments, to investigate the role of and molecular mechanisms through which TRIM11 contributes to EC progression, and evaluate its potential as a candidate marker associated with adverse clinicopathological features. Transcriptomic analysis was conducted using data from TCGA, GTEx, CCLE, and other publicly available databases to assess TRIM11 expression and its correlation with clinicopathological features, immune infiltration and TRIM11’s relationship with treatment response in EC. In vitro experiments showed that TRIM11 overexpression significantly promoted EC cell proliferation, migration, and invasion. Flow cytometry analysis revealed that TRIM11 increased the proportion of cells entering the S phase. Mechanistically, co-immunoprecipitation assays demonstrated that endogenous TRIM11 directly interacted with Axin2 and GSK3β, two core components of the β-catenin destruction complex. Additionally, TRIM11 knockdown altered the expression of key proteins in the β-catenin signaling pathway, including CyclinD1, GSK3β, Axin2, and β-catenin. Collectively, these findings highlight TRIM11 as a pro-oncogenic factor and suggest that it is a potential functional driver of EC.