MicroRNA-939 inhibits cell proliferation via targeting LRSAM1 in Hirschsprung's disease

Guanglin Chen1,2, Chunxia Du1,2, Ziyang Shen1,2,3

  • 1State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 211166, China.

Aging
|December 19, 2017
PubMed

Insights

Hirschsprung

Area of Science:

  • Gastroenterology
  • Developmental Biology
  • Molecular Biology

Background:

  • Hirschsprung's disease (HSCR) is a congenital digestive disorder stemming from defective neural crest cell development.
  • MicroRNAs (miRNAs) are implicated in various diseases, but their specific role in HSCR requires further elucidation.
  • Understanding miRNA involvement is crucial for advancing HSCR research.

Purpose of the Study:

  • To investigate the role of miR-939 in Hirschsprung's disease.
  • To explore the relationship between miR-939 and LRSAM1 in HSCR.
  • To examine the impact of miR-939 on cellular functions and autophagy in HSCR.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunoblot analyses were used to assess miR-939 and LRSAM1 expression in HSCR tissues.
  • Cellular assays (CCK-8, transwell, flow cytometry) were performed to evaluate miR-939 function.
  • Dual-luciferase reporter assays validated the interaction between miR-939 and LRSAM1, while immunoblotting assessed autophagy levels.

Main Results:

  • miR-939 was significantly upregulated, and LRSAM1 expression was decreased in HSCR tissues.
  • Overexpression of miR-939 inhibited cell proliferation but did not affect apoptosis or cell cycle.
  • LRSAM1 showed similar functional effects, and autophagy was impaired in HSCR tissues; miR-939 did not inhibit autophagy despite downregulating LRSAM1.

Conclusions:

  • miR-939 may play a role in HSCR by regulating LRSAM1.
  • Impaired autophagy is observed in HSCR, suggesting its potential contribution to the disease.
  • Further research into miR-939 and autophagy could offer new insights into HSCR pathogenesis.

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