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MiR-329-3p inhibits hepatocellular carcinoma cell proliferation and migration through USP22-Wnt/β-Catenin pathway

R-Q Xin1, W-B Li, Z-W Hu

  • 1Department of Hepatobiliary Surgery, Inner Mongolia People's Hospital, Hohhot, Inner Mongolia, P.R. China. sunwei85@pumch.cn.

European Review for Medical and Pharmacological Sciences
|October 22, 2020
PubMed
Abstract

Insights

MicroRNA-329-3p (miR-329-3p) is downregulated in hepatocellular carcinoma. It inhibits cancer cell proliferation and migration by targeting USP22 and the Wnt/β-Catenin pathway, offering potential therapeutic insights.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • MicroRNA-329-3p (miR-329-3p) involvement in tumorigenesis is known, but its specific role in hepatocellular carcinoma (HCC) remains unexplored.
  • Hepatocellular carcinoma is a significant global health concern with a need for novel therapeutic targets.

Purpose of the Study:

  • To investigate the effect of miR-329-3p on hepatocellular carcinoma development.
  • To elucidate the underlying molecular mechanism of miR-329-3p in HCC progression.

Main Methods:

  • Quantitative real-time PCR and Western blot to assess gene and protein expression in HCC tissues and cells.
  • Cell proliferation (CCK-8) and migration (Transwell) assays to evaluate functional effects.
  • Dual-Luciferase reporter gene assay to confirm direct targeting of USP22 by miR-329-3p.

Main Results:

  • miR-329-3p expression was significantly reduced in HCC tissues compared to adjacent normal tissues.
  • Overexpression of miR-329-3p suppressed proliferation and migration of HepG2 HCC cells.
  • miR-329-3p directly targets USP22, inhibiting HepG2 cell proliferation and migration.
  • USP22 activates the Wnt/β-Catenin pathway, influencing HCC cell behavior.

Conclusions:

  • miR-329-3p acts as a tumor suppressor in HCC by inhibiting the USP22-Wnt/β-Catenin pathway.
  • This study reveals a novel mechanism for miR-329-3p in HCC, suggesting its potential as a therapeutic target.

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