LINC00265 maintains hepatocyte proliferation during liver regeneration by targeting miRNA-28-5p

Biosci Biotechnol Biochem. 2021 Feb 24;85(3):528-536. doi: 10.1093/bbb/zbaa049.

Abstract

Long noncoding RNAs have been implicated in many biological processes, but their roles in liver regeneration still need to be illustrated. Therefore, we aimed to investigate the role of LINC00265 as a pivotal regulator of hepatocyte proliferation during liver regeneration. It was found that LINC00265 is significantly upregulated in rat liver tissues at various time points after 2/3 liver resection. LINC00265 knockdown inhibited hepatocyte proliferation, induced cell apoptosis and led to G2/M phase cell cycle arrestment. In rats subjected to surgery, LINC00265 knockdown decreased liver/body weight ratio, attenuated improvement from liver damage and reduced Ki67 and PCNA expression. Luciferase reporter assays confirmed that miR-28-5p was a direct target of LINC00265, and inhibition of miR-28-5p abolished the effect of LINC00265 knockdown. In summary, LINC00265 might maintain hepatocyte proliferation by targeting miR-28-5p during liver regeneration and should be considered as a promising therapeutic option for hepatocyte regeneration after liver resection.

Keywords: LINC00265; cell proliferation; liver regeneration; long noncoding RNA; miRNA-28-5p.

MeSH terms

  • Apoptosis / genetics
  • Cell Line
  • Cell Proliferation / physiology*
  • Gene Knockdown Techniques
  • Hepatocytes / cytology*
  • Hepatocytes / metabolism
  • Humans
  • Ki-67 Antigen / metabolism
  • Liver Regeneration*
  • MicroRNAs / physiology*
  • Proliferating Cell Nuclear Antigen / metabolism
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*

Substances

  • Ki-67 Antigen
  • MIRN28 microRNA, human
  • MicroRNAs
  • Proliferating Cell Nuclear Antigen
  • RNA, Long Noncoding