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The Role of the MiR-181 Family in Hepatocellular Carcinoma

Jinbiao Chen1, Ken Liu1,2, Mathew A Vadas3

  • 1Liver Injury and Cancer Program, Cancer Innovations Centre, Centenary Institute, Sydney Medical School, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2050, Australia.

Cells
|August 9, 2024
PubMed

Insights

MicroRNAs-181 (miR-181) are elevated in some liver cancer tissues, promoting tumor progression by inducing epithelial-mesenchymal transition. Understanding miR-181

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Hepatocellular carcinoma (HCC) is a leading cause of cancer death globally, necessitating novel systemic treatments.
  • MicroRNAs (miRNAs) are increasingly recognized as key players in hepatocarcinogenesis.
  • The microRNA-181 (miR-181) family is upregulated in some cirrhotic and HCC tissues, driving tumor progression.

Purpose of the Study:

  • To review the roles of miR-181 family members in hepatocellular carcinoma.
  • To explore miR-181 targets and their modulation of signaling pathways.
  • To discuss factors regulating miR-181 expression and function in HCC.

Main Methods:

  • Literature review of studies on miR-181 in HCC.
  • Analysis of molecular mechanisms involving miR-181.
  • Synthesis of current knowledge on miR-181's role in hepatocarcinogenesis.

Main Results:

  • miR-181 family members are upregulated in a subset of HCC tissues.
  • Upregulation of miR-181 induces epithelial-mesenchymal transition (EMT), promoting HCC progression.
  • miR-181 influences the function of various cell types, including endothelial and immune cells.

Conclusions:

  • miR-181 plays a significant role in HCC development and progression.
  • Further research into miR-181 pathways could reveal therapeutic targets for HCC.
  • Understanding miR-181 regulation and function is crucial for advancing HCC treatment strategies.
Keywords:
Akt pathwayCbx7MAPK pathwayTGF-betaanti-miRmicroRNA knockoutmicroRNA targetsnon-coding RNAtranscriptional regulation

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