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MicroRNA-223: a key regulator of liver tumour microenvironment
  1. Matias A Avila1,2,3,4
  1. 1 Hepatology Program, Cima. University of Navarra, Pamplona, Spain
  2. 2 Centro de Investigación Biomédica en Red. Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain
  3. 3 Instituto de Investigaciones Sanitarias de Navarra (IdiSNA), Pamplona, Spain
  4. 4 Cancer Center Clinica Universidad de Navarra (CCUN), Pamplona, Spain
  1. Correspondence to Professor Matias A Avila, Hepatology, University of Navarra, Pamplona, Navarra, Spain; maavila{at}

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Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related deaths worldwide with few effective drug treatments. Recent combination therapies inhibiting immune checkpoints and angiogenesis showed better overall and progression-free survival outcomes than the protein kinase inhibitor sorafenib in patients with unresectable HCC,1 suggesting targeting tumour microenvironment (TME) is a promising strategy for the treatment of HCC. However, how the TME is developed and regulated is still poorly known. Thus, understanding the pathogenesis of HCC TME would be essential in order to develop more effective HCC therapies.

In Gut, Fu et al 2 have demonstrated that microRNA-223 (miR-223) is a key regulator of HCC TME by modulating tumour hypoxic microenvironment, immunosuppression and angiogenesis. miRNAs are a class of small (~19 to 24 nucleotides in length) endogenous RNAs that play critical roles in controlling the development, progression and prognosis of liver disease.3 miR-223 is a well-documented myeloid-enriched miRNA that is expressed at the highest levels in neutrophils, followed by macrophages, but present at low levels in hepatocytes. Relevantly, miR-223 acts as an important feedback inhibitor to ameliorate liver inflammation by …

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  • Contributors MAA wrote the article.

  • Funding Author’s research is supported by a grant from FEDER/Ministerio de Ciencia, Innovación y Universidades-Agencia Estatal de Investigación, Spain (grant number PID2019-104878RB-100) and the Eugenio Rodriguez-Pascual Foundation, and also received the generous support of Mr Eduardo Avila.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

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