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12:06

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Published on: October 10, 2011

BEND3 promotes hepatocellular carcinoma progression and metastasis by activating the PI3K/AKT/mTOR pathway and

Liu-Lin Yang1, Xing Chen2, Kai-Ting Huang1

  • 1Department of Hepatological Surgery, Guangxi Medical University First Affiliated Hospital, China.

Clinics and Research in Hepatology and Gastroenterology
|March 30, 2025
PubMed
Abstract

Insights

High BEND3 expression in hepatocellular carcinoma (HCC) promotes cancer growth and spread. This study reveals BEND3 drives HCC progression by activating the PI3K/AKT/mTOR pathway and inducing epithelial-mesenchymal transition (EMT).

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Hepatocellular carcinoma (HCC) is a major global health concern with limited therapeutic options.
  • Understanding the molecular drivers of HCC progression is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of BEND3 in HCC.
  • To correlate BEND3 expression with clinical characteristics.
  • To elucidate the functional and mechanistic impacts of BEND3 on HCC progression.

Main Methods:

  • Bioinformatics analysis, qRT-PCR, western blotting, and immunohistochemistry were used to assess BEND3 expression.
  • Functional assays (CCK-8, colony formation, wound healing, Transwell) evaluated proliferation, migration, and invasion.
  • Immunofluorescence and western blotting analyzed the PI3K/AKT/mTOR pathway and epithelial-mesenchymal transition (EMT).

Main Results:

  • BEND3 expression is significantly elevated in HCC tissues and associated with poor prognosis.
  • BEND3 overexpression promotes HCC cell proliferation, migration, and invasion.
  • BEND3 induces EMT and activates the PI3K/AKT/mTOR signaling pathway in HCC.

Conclusions:

  • BEND3 is a key driver of HCC progression.
  • BEND3 enhances HCC aggressiveness through EMT induction and PI3K/AKT/mTOR pathway activation.
  • Targeting BEND3 may offer a therapeutic strategy for HCC.
Keywords:
BEND3EMTHepatocellular carcinomaPI3K/AKT/mTORProliferation and migration

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