MiR-195 affects cell migration and cell proliferation by down-regulating DIEXF in Hirschsprung's disease

Hao Lei, Junwei Tang, Hongxing Li

  • 1State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 211166, China. twbcn@163.com.

BMC Gastroenterology
|July 11, 2014
PubMed
Abstract

Insights

MicroRNA-195 (miR-195) is elevated in Hirschsprung's disease (HSCR), a congenital gut motility disorder. Higher miR-195 levels suppress DIEXF, impairing cell function and contributing to HSCR pathogenesis.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Developmental Biology

Background:

  • Hirschsprung's disease (HSCR) is the leading congenital disorder affecting gut motility.
  • Investigating the specific molecular mechanisms underlying HSCR pathogenesis is crucial for understanding and potentially treating this condition.

Purpose of the Study:

  • To elucidate the role of microRNA-195 (miR-195) in the development of Hirschsprung's disease.
  • To determine the relationship between miR-195 expression and its target gene, DIEXF, in HSCR.

Main Methods:

  • Quantitative analysis of miRNA, mRNA, and protein expression in colon tissues from HSCR patients (n=78) and controls (n=66).
  • In vitro functional assays including Transwell migration, Cell Counting Kit-8 (CCK-8) for proliferation, and flow cytometry were performed.
  • Investigated the regulatory effect of miR-195 on DIEXF expression in cellular models.

Main Results:

  • Expression levels of miR-195 were significantly elevated in HSCR patients compared to controls.
  • Aberrantly lower expression levels of digestive-organ expansion factor (DIEXF) were observed in HSCR tissues.
  • Increased miR-195 suppressed DIEXF levels in cells, leading to impaired cell migration and proliferation.

Conclusions:

  • Aberrant upregulation of miR-195 is implicated in Hirschsprung's disease pathogenesis.
  • Downregulation of DIEXF by miR-195 contributes to the cellular dysfunction observed in HSCR.
  • miR-195 represents a potential molecular target for understanding and managing HSCR.

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