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Updated: Aug 24, 2025

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The m6A-methylated mRNA pattern and the activation of the Wnt signaling pathway under the hyper-m6A-modifying

Can-Xiang Lin1, Zhi-Jing Chen1, Qi-Lin Peng2

  • 1Key Laboratory of Regenerative Medicine, Ministry of Education, Department of Plastic Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, China.

Frontiers in Cell and Developmental Biology
|October 20, 2022
PubMed

Insights

Keloid pathogenesis involves altered RNA methylation patterns. Hyper-methylation of the Wnt/β-catenin pathway in dermal fibroblasts promotes keloid development.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Dermatology

Background:

  • Keloids are abnormal scars resulting from excessive fibroblast activity.
  • The role of RNA modifications, specifically N6-methyladenosine (m6A), in keloid pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the global m6A-modified RNA patterns in keloid tissues.
  • To elucidate the underlying mechanisms, particularly the involvement of the Wnt signaling pathway, in keloid development.

Main Methods:

  • Comparative analysis of m6A modification patterns and gene expression between keloid and normal skin tissues using MeRIP sequencing and RNA sequencing.
  • Validation of key molecular changes using Western blotting and immunofluorescence staining.

Main Results:

  • Keloid tissues exhibit significantly higher m6A modification levels and distinct m6A-associated gene profiles compared to normal skin.
  • Upregulated differentially expressed genes and m6A-modified genes are predominantly linked to the Wnt signaling pathway.
  • Hyper-methylation and activation of the Wnt/β-catenin pathway were confirmed in keloid fibroblasts.

Conclusions:

  • Fibroblasts in keloid tissues are characterized by a cellular hyper-m6A-methylated state.
  • The hyper-m6A-modified and highly expressed Wnt/β-catenin pathway in dermal fibroblasts likely drives keloid pathogenesis.
Keywords:
RNA sequencingfibroblastskeloidm6A modificationthe Wnt signaling pathway

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