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METTL3 contributes to slow transit constipation by regulating miR-30b-5p/PIK3R2/Akt/mTOR signaling cascade through

Wen-Jing Gong1, Rong Li2, Qiao-Qiong Dai1

  • 1General Surgery, Cancer Center, Department of Colorectal Surgery, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Zhejiang, China.

Journal of Gastroenterology and Hepatology
|September 6, 2022
PubMed
Abstract

Insights

Methyltransferase-like 3 (METTL3) promotes cell death in slow transit constipation (STC) by regulating miR-30b-5p and PIK3R2. METTL3 may be a therapeutic target for STC.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) is a key RNA modification.
  • Methyltransferase-like 3 (METTL3) is crucial for cellular functions.
  • The role of METTL3 in slow transit constipation (STC) remains unclear.

Purpose of the Study:

  • Investigate the role of m6A methylase METTL3 in STC.
  • Elucidate the molecular mechanisms by which METTL3 affects interstitial cells of Cajal (ICCs) in STC.

Main Methods:

  • Measured METTL3, DGCR8, and miR-30b-5p expression in STC tissues and ICCs.
  • Performed loss-of-function analyses on METTL3, miR-30b-5p, and DGCR8 in ICCs.
  • Utilized luciferase reporter assays to confirm miR-30b-5p binding to PIK3R2.

Main Results:

  • METTL3, DGCR8, miR-30b-5p, and m6A levels were elevated in STC tissues and ICCs.
  • METTL3 and miR-30b-5p silencing reduced apoptosis, autophagy, and pyroptosis in ICCs.
  • METTL3 accelerates pri-miR-30b-5p maturation via m6A, reducing PIK3R2 and inhibiting the PI3K/Akt/mTOR pathway, leading to ICC death.

Conclusions:

  • METTL3 promotes apoptosis, autophagy, and pyroptosis in ICCs via the DGCR8/miR-30b-5p/PIK3R2 axis in an m6A-dependent manner.
  • METTL3 plays a significant role in the pathogenesis of STC.
  • METTL3 emerges as a potential therapeutic target for STC.
Keywords:
Functional constipationICCsMETTL3PIK3R2Slow transit constipationmiR-30b-5p

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