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IFN-treated macrophage-derived exosomes prevents HBV-HCC migration and invasion via regulating

Jing Chen1,2,3, Qi Yin2,3, Shiheng Xu2

  • 1Department of Pulmonary and Critical Care Medicine, Yunnan Provincial Key Laboratory for Clinical Virology, Institute of Basic and Clinical Medicine, The First People's Hospital of Yunnan Province, Kunming, China.

Frontiers in Cellular and Infection Microbiology
|November 12, 2024
PubMed
Abstract

Insights

Interferon-alpha-induced exosomes (IFN-exo) deliver miR-106b-3p, which inhibits hepatitis B virus (HBV) replication and hepatocellular carcinoma (HCC) cell migration by targeting PCGF3. This miR-106b-3p/PCGF3 axis offers potential biomarkers for HBV-HCC prevention and treatment.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Oncology

Background:

  • Exosomes derived from interferon-alpha-treated liver non-parenchymal cells (IFN-exo) exhibit antiviral properties.
  • The role of miR-106b-3p in hepatitis B virus-related hepatocellular carcinoma (HBV-HCC) and its underlying mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the role of miR-106b-3p delivered by IFN-exo in HBV-HCC.
  • To elucidate the mechanism by which miR-106b-3p affects HBV replication and HCC progression.

Main Methods:

  • Huh7 cells (HBV-C2 and B3 transfected) were co-cultured with IFN-exo.
  • miR-106b-3p, HBsAg, HBeAg, and HBV DNA levels were measured.
  • Cell proliferation, apoptosis, migration, and invasion were analyzed.
  • Dual-luciferase reporter assay identified PCGF3 as a direct target of miR-106b-3p.
  • Western blot assessed protein expression related to PCGF3 and the PI3K/AKT pathway.
  • PCGF3 mRNA expression was analyzed in HCC patient tissues.

Main Results:

  • IFN-exo treatment significantly increased miR-106b-3p expression in cells and supernatants.
  • miR-106b-3p overexpression in Huh7-C2/B3 cells reduced HBsAg and HBV DNA levels.
  • miR-106b-3p directly targets and downregulates PCGF3 expression.
  • IFN-exo, miR-106b-3p, or siRNAs-PCGF3 inhibited cell migration and invasion, suppressing the PI3K/AKT pathway.
  • PCGF3 expression was lower in HBeAg-positive HCC tissues compared to HBeAg-negative tissues.

Conclusions:

  • Macrophage-derived miR-106b-3p delivered by IFN-exo inhibits HBV replication and HCC cell migration/invasion by regulating the PCGF3/PI3K/AKT signaling axis.
  • miR-106b-3p and PCGF3 are potential biomarkers for the prevention and treatment of HBV-HCC.
Keywords:
HBV-related hepatocellular carcinomaIFN-α-induced macrophage-derived exosomePCGF3PI3K/AKT pathwaymiR-106b-3p

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