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MCM3 promotes hepatocellular carcinoma progression via Epithelial-mesenchymal Transition through AKT/Twist signaling

Wei-Guo Tang1, Jin-Feng Feng1, Xian Li2

  • 1Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai 201199, China; Key laboratory of whole-period monitoring and precise intervention of digestive cancer (SMHC), Minhang Hospital, Fudan University, Shanghai 201199, China.

Annals of Hepatology
|February 20, 2025
PubMed
Summary

Minichromosome maintenance complex component 3 (MCM3) drives hepatocellular carcinoma (HCC) progression by promoting cell migration and invasion. MCM3 expression is a prognostic marker, and targeting it may offer new HCC therapies.

Keywords:
AKT/Twist pathwayEpithelial–mesenchymal transitionHepatocellular carcinomaMCM3Prognostic biomarker

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Hepatocellular carcinoma (HCC) is a major cause of cancer death with high recurrence and metastasis rates.
  • Novel prognostic markers and therapeutic strategies are needed for HCC management.
  • The role of Minichromosome maintenance complex component 3 (MCM3) in HCC is not well understood.

Purpose of the Study:

  • To investigate the expression and function of MCM3 in hepatocellular carcinoma.
  • To explore the prognostic significance of MCM3 in HCC patients.
  • To elucidate the underlying molecular mechanisms by which MCM3 influences HCC progression.

Main Methods:

  • Analysis of MCM3 expression in HCC cell lines and patient tissues.
  • In vitro and in vivo functional assays to assess MCM3's role in proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).
  • Exploration of signaling pathways, including AKT and Twist, involved in MCM3-mediated effects.

Main Results:

  • Elevated MCM3 expression was observed in HCC cell lines and patient samples.
  • Higher MCM3 levels correlated with microvascular invasion, advanced stage, and poorer survival.
  • MCM3 promoted HCC cell proliferation, migration, invasion, and EMT in vitro, and accelerated tumor growth in vivo, via the AKT/Twist pathway.

Conclusions:

  • MCM3 acts as an oncogenic factor in HCC, driving disease progression.
  • MCM3 expression serves as a valuable prognostic indicator for HCC.
  • Targeting MCM3 presents a potential novel therapeutic strategy for hepatocellular carcinoma.