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MicroRNA-181a inhibits autophagy by targeting Atg5 in hepatocellular carcinoma

Jun Yang1, Youzhao He2, Niankuan Zhai2

  • 1Department of General Surgery, Shanghai First People's Hospital, Nanjing Medical University, Nanjing, China.

Frontiers in Bioscience (Landmark Edition)
|September 21, 2017
PubMed

Insights

MicroRNA-181a inhibits autophagy in hepatocellular carcinoma (HCC) by targeting Atg5. This leads to reduced apoptosis and increased tumor growth, suggesting miR-181a as a potential therapeutic target for HCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Autophagy acts as a tumor suppressor in chronic liver disease and cirrhosis, with deficiency potentially leading to hepatocellular carcinoma (HCC).
  • MicroRNA-181a has been implicated in the regulation of various tumor types, but its specific role in HCC autophagy is not well understood.

Purpose of the Study:

  • To investigate the role of microRNA-181a (miR-181a) in the regulation of autophagy within hepatocellular carcinoma (HCC).

Main Methods:

  • Comparative analysis of miR-181a mRNA expression and autophagy levels in human HCC versus normal liver tissue.
  • Luciferase assay to confirm the interaction between miR-181a and its target gene, Atg5.
  • Assessment of apoptosis and tumor growth in HepG2 cells and a HepG2 xenograft model using an miR-181a sponge.

Main Results:

  • miR-181a mRNA expression was elevated, while autophagy levels were decreased in human HCC tissues compared to normal liver tissue.
  • Atg5 was identified as a direct target gene of miR-181a via luciferase assay.
  • Upregulation of an miR-181a sponge led to increased apoptosis in HepG2 cells and suppressed tumor growth in vivo.

Conclusions:

  • miR-181a inhibits autophagy in HCC by targeting Atg5.
  • This inhibition of autophagy by miR-181a results in decreased apoptosis and promotes tumor growth in HCC.
  • These findings highlight miR-181a as a potential therapeutic target for managing hepatocellular carcinoma.

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