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YTHDF1-mediated translation amplifies Wnt-driven intestinal stemness.

Bing Han1, Sujun Yan1, Saisai Wei1

  • 1Institute of Environmental Medicine, Sir Run-Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.

EMBO Reports
|February 18, 2020
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Summary
This summary is machine-generated.

YTHDF1, an m6A reader, amplifies Wnt signaling in intestinal stem cells (ISCs). Targeting YTHDF1 inhibits ISC regeneration and tumor growth, highlighting its role in stemness and Wnt pathway regulation.

Keywords:
Wnt signalingYTHDF1intestinal stem cellm6Atumorigenesis

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • N6-methyladenosine (m6A) mRNA methylation regulates gene expression.
  • The role of m6A in intestinal stem cell (ISC) homeostasis is largely unknown.
  • YTHDF1 is an m6A reader protein.

Purpose of the Study:

  • To investigate the role of YTHDF1 in ISC homeostasis.
  • To determine the mechanism by which YTHDF1 affects Wnt signaling.
  • To evaluate YTHDF1 as a therapeutic target in intestinal regeneration and tumorigenesis.

Main Methods:

  • Analysis of YTHDF1 expression in ISCs.
  • Genetic ablation of Ythdf1 in mice.
  • Assessment of Wnt-driven regeneration and tumorigenesis.
  • Investigation of YTHDF1's effect on Wnt signaling effectors' translation.
  • Evaluation of YTHDF1 targeting in established tumors.

Main Results:

  • YTHDF1 is highly expressed in ISCs and upregulated by Wnt signaling.
  • Ythdf1 ablation blocks Wnt-driven regeneration and tumorigenesis, reducing ISC stemness.
  • YTHDF1 facilitates translation of Wnt effectors like TCF7L2/TCF4.
  • Targeting YTHDF1 in established tumors causes shrinkage and prolongs survival.

Conclusions:

  • YTHDF1 acts as an amplifier of Wnt/β-catenin signaling at the translational level.
  • YTHDF1 is essential for ISC maintenance during regeneration and tumorigenesis.
  • YTHDF1 is a potential therapeutic target for intestinal cancers and regenerative medicine.