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Abstract <p>Tripartite motif containing 56 (TRIM56) has been implicated in tumor development, but its role in esophageal cancer remains unclear. The aim of this study was to determine the correlation between TRIM56 expression and clinicopathological characteristics in esophageal cancer, and investigate the influence of TRIM56 expression on autophagy. Then, we examined TRIM56 expression in esophageal cancer, and TRIM56 expression was upregulated in both esophageal cancer tissues and cells. The upregulated TRIM56 expression was strongly correlated with tumor size, degree of differentiation, and TNM stage. Additionally, Well-differentiated esophageal cancer exhibited TRIM56 upregulation. <i>TRIM56</i> knockdown upregulated the expression levels of LC3 and ATG12, downregulated the expression of p62, and increased the autophagic flux in Eca109 cells. The findings of this study indicated that TRIM56 inhibits autophagy and that TRIM56 expression is closely related to some clinicopathological characteristics in esophageal cancer. Thus, TRIM56 is a potential novel prognostic biomarker and a promising therapeutic target for esophageal cancer.</p>

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TRIM56 Mediates Autophagy Inhibition in Esophageal Cancer

  • 期刊论文

  • 发表日期：

    2025年5月11日

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  • J. Gao,
  • R. Z. Li,
  • H. Peng,
  • S. M. Al-Harazi,
  • S. G. Luo,
  • H. M. Hua,
  • Y. Y. Yang,
  • F. L. Wang,
  • J. P. Wang

摘要

Abstract

Tripartite motif containing 56 (TRIM56) has been implicated in tumor development, but its role in esophageal cancer remains unclear. The aim of this study was to determine the correlation between TRIM56 expression and clinicopathological characteristics in esophageal cancer, and investigate the influence of TRIM56 expression on autophagy. Then, we examined TRIM56 expression in esophageal cancer, and TRIM56 expression was upregulated in both esophageal cancer tissues and cells. The upregulated TRIM56 expression was strongly correlated with tumor size, degree of differentiation, and TNM stage. Additionally, Well-differentiated esophageal cancer exhibited TRIM56 upregulation. TRIM56 knockdown upregulated the expression levels of LC3 and ATG12, downregulated the expression of p62, and increased the autophagic flux in Eca109 cells. The findings of this study indicated that TRIM56 inhibits autophagy and that TRIM56 expression is closely related to some clinicopathological characteristics in esophageal cancer. Thus, TRIM56 is a potential novel prognostic biomarker and a promising therapeutic target for esophageal cancer.