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<p>Pancreatic adenocarcinoma remains one of the most challenging malignancies in oncology, characterized by its exceptionally high mortality rate. TRIM56 (Tripartite Motif Containing 56) has demonstrated significant roles in various cancer types, yet its biological functions in pancreatic cancer remain largely unexplored. This study investigates the expression patterns and functional significance of TRIM56 in pancreatic tumor development and progression. Gene Expression Profiling Interactive Analysis (GEPIA) and Kaplan–Meier (K-M) plotter analyses were conducted on The Cancer Genome Atlas-Pancreatic Adenocarcinoma (TCGA-PRAD) datasets. We measured TRIM56 levels in pancreatic tumor samples and cell cultures through quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and Western blotting. Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EDU), and Transwell assays were employed to evaluate how TRIM56 knockdown affected cellular proliferation, migration, and invasion capabilities. Overexpression in normal pancreatic duct epithelial (HPDE) cells was also performed to assess oncogenic potential of TRIM56. Animal studies utilized both subcutaneous xenograft and liver metastasis models in nude mice to evaluate the impacts of TRIM56 knockdown on tumor growth and metastatic potential. Pancreatic cancer tissues and cell lines exhibited significantly elevated TRIM56 expression. Higher TRIM56 expression was linked to shorter survival times in patients with pancreatic cancer. Reducing TRIM56 expression in BxPC-3 and PANC-1 cells significantly inhibited proliferation, migration, and invasion. At the molecular level, TRIM56 silencing decreased the expression of Tumor Necrosis Factor Receptor-Associated Factor 6 (TRAF6) and inhibited the activation of Nuclear Factor kappa B (NF-κB), suggesting their role in TRIM56's cancer-promoting effects. Overexpression of TRIM56 in normal pancreatic epithelial cells promoted cellular aggressiveness. In xenograft models, TRIM56 knockdown resulted in reduced tumor volume and diminished liver metastases. TRIM56 promotes pancreatic cancer progression through activation of the TRAF6/NF-κB signaling pathway. Targeting TRIM56 represents a promising therapeutic strategy for pancreatic cancer treatment.</p>

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The oncogenic role of TRIM56 in pancreatic cancer via the TRAF6/NF-kB axis

  • 期刊论文

  • 发表日期：

    2025年6月21日

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  • Chenglin Jiang,
  • Haitao Li,
  • Dazhou Li,
  • Xinxin Li,
  • Shengzheng Luo,
  • Liusheng You

摘要

Pancreatic adenocarcinoma remains one of the most challenging malignancies in oncology, characterized by its exceptionally high mortality rate. TRIM56 (Tripartite Motif Containing 56) has demonstrated significant roles in various cancer types, yet its biological functions in pancreatic cancer remain largely unexplored. This study investigates the expression patterns and functional significance of TRIM56 in pancreatic tumor development and progression. Gene Expression Profiling Interactive Analysis (GEPIA) and Kaplan–Meier (K-M) plotter analyses were conducted on The Cancer Genome Atlas-Pancreatic Adenocarcinoma (TCGA-PRAD) datasets. We measured TRIM56 levels in pancreatic tumor samples and cell cultures through quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and Western blotting. Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EDU), and Transwell assays were employed to evaluate how TRIM56 knockdown affected cellular proliferation, migration, and invasion capabilities. Overexpression in normal pancreatic duct epithelial (HPDE) cells was also performed to assess oncogenic potential of TRIM56. Animal studies utilized both subcutaneous xenograft and liver metastasis models in nude mice to evaluate the impacts of TRIM56 knockdown on tumor growth and metastatic potential. Pancreatic cancer tissues and cell lines exhibited significantly elevated TRIM56 expression. Higher TRIM56 expression was linked to shorter survival times in patients with pancreatic cancer. Reducing TRIM56 expression in BxPC-3 and PANC-1 cells significantly inhibited proliferation, migration, and invasion. At the molecular level, TRIM56 silencing decreased the expression of Tumor Necrosis Factor Receptor-Associated Factor 6 (TRAF6) and inhibited the activation of Nuclear Factor kappa B (NF-κB), suggesting their role in TRIM56's cancer-promoting effects. Overexpression of TRIM56 in normal pancreatic epithelial cells promoted cellular aggressiveness. In xenograft models, TRIM56 knockdown resulted in reduced tumor volume and diminished liver metastases. TRIM56 promotes pancreatic cancer progression through activation of the TRAF6/NF-κB signaling pathway. Targeting TRIM56 represents a promising therapeutic strategy for pancreatic cancer treatment.