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Related Experiment Video

Updated: Nov 24, 2025

Transcorporal Artificial Urinary Sphincter Cuff Placement in a Case Requiring Revision for Urethral Atrophy
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Erratum.

Kairui Liu1, Xiaolin Wu1, Xian Zang2

  • 1Department of Hepatobiliary Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen UniversityGuangzhou, Guangdong ProvinceP.R. China.

Oncology Research
|December 22, 2020
PubMed
Summary

Tumor necrosis factor receptor-associated factor 4 (TRAF4) promotes hepatocellular carcinoma (HCC) cell migration and invasion. TRAF4 activates the PI3K/Akt pathway, driving epithelial-mesenchymal transition (EMT) and metastasis in HCC.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Tumor necrosis factor receptor-associated factor 4 (TRAF4) is overexpressed in various cancers, potentially promoting tumor progression.
  • The specific role of TRAF4 in hepatocellular carcinoma (HCC) has not been fully elucidated.

Purpose of the Study:

  • To investigate the role and mechanism of TRAF4 in hepatocellular carcinoma (HCC) progression.
  • To determine the association between TRAF4 expression and clinicopathological features of HCC.

Main Methods:

  • Quantitative analysis of TRAF4 expression in HCC cell lines and tissues.
  • In vitro assays for cell migration and invasion.
  • In vivo metastasis models in nude mice.
  • Western blot analysis to assess protein phosphorylation and expression (Akt, Slug, E-cadherin, vimentin).
  • Pharmacological inhibition (LY294002) and genetic manipulation (Akt1) of the PI3K/Akt pathway.

Main Results:

  • TRAF4 was significantly overexpressed in HCC tissues and cell lines compared to normal controls.
  • TRAF4 overexpression correlated with increased tumor quantity and vascular invasion in HCC patients.
  • TRAF4 enhanced HCC cell migration, invasion, and metastasis in vitro and in vivo.
  • TRAF4 promoted epithelial-mesenchymal transition (EMT) by upregulating p-Akt and Slug, downregulating E-cadherin, and upregulating vimentin.
  • Silencing TRAF4 reversed these EMT-associated changes, while PI3K/Akt pathway modulation affected TRAF4's impact.

Conclusions:

  • TRAF4 plays a crucial role in promoting HCC cell migration, invasion, and metastasis.
  • TRAF4 facilitates HCC progression through the activation of the PI3K/Akt signaling pathway, leading to EMT.
  • TRAF4 represents a potential therapeutic target for inhibiting HCC metastasis.