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Correlations of m6A methylation-related mRNAs with thyroid cancer
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  • Published: 19 January 2026

Correlations of m6A methylation-related mRNAs with thyroid cancer

  • Zhen Jiang1,2,3,4,5,6 na1,
  • Sheng Luo7 na1,
  • Yingruo Lin1 na1,
  • Huihao Zhang8 &
  • …
  • Ruhai Yi1,2,3,4,5,6 

Scientific Reports , Article number:  (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Abstract

N6-methyladenosine (m6A) RNA methylation plays a crucial role in tumorigenesis. However, the specific role of m6A modifications in the malignant progression of papillary thyroid carcinoma (PTC) without autoimmune thyroid disease (AITD) remains unclear. We analyzed a randomly selected subset of three pairs from a total cohort of 26 pairs of cancerous and para-cancerous tissues from patients with PTC without AITD to investigate global m6A levels and the gene expression of key factors driving m6A methylation. Our results revealed a significant increase in global m6A methylation in cancerous tissues, accompanied by upregulation of the m6A “reader” gene IGF2BP2. Of the 486 upregulated and 39 downregulated genes identified in cancerous tissues, most of the top-enriched pathways were associated with activated genes and contributed to cancer progression. A significant protein–protein interaction between IGF2BP2 and several key cancer-related genes, particularly FN1 and LAMB3, was observed. Moreover, 313 mRNAs, 55 lncRNAs, and 8 ncRNAs exhibited significant m6A methylation differences, overlapping with differentially expressed cancer-associated genes, particularly NUM, which was recently identified as a potential biomarker for PTC. These findings underscore the importance of m6A-related mechanisms and functions in PTC without AITD development and suggest that FN1-, NMU-, and LAMB3-associated pathways may be potential therapeutic targets and molecular mechanisms for this disease.

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Data availability

The datasets generated during the current study are available in the Gene Expression Omnibus (GEO) repository, under accession number [GSE287426].

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Acknowledgements

We are grateful to the patients for their help and willingness to participate in this study. This study was supported by the Natural Science Foundation of the Fujian Province (Grant Number: 2022J01222) and the Fujian Provincial Health Commission Youth Scientific Research Project (Grant Number: 2023QNA037).

Funding

This study was funded by Natural Science Foundation of Fujian Province (2022J01222), Fujian Provincial Health Commission Youth Scientific Research Project (2023QNA037).The funding body had no further role in the study design, decision to publish or preparation of manuscript.

Author information

Author notes

  1. Zhen Jiang, Sheng Luo and Yingruo Lin contributed equally to this work.

Authors and Affiliations

  1. Department of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China

    Zhen Jiang, Yingruo Lin & Ruhai Yi

  2. Department of Endocrinology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, 350212, China

    Zhen Jiang & Ruhai Yi

  3. Clinical Research Center for Metabolic Diseases of Fujian Province, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China

    Zhen Jiang & Ruhai Yi

  4. Fujian Key Laboratory of Glycolipid and Bone Mineral Metabolism, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China

    Zhen Jiang & Ruhai Yi

  5. Diabetes Research Institute of Fujian Province, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China

    Zhen Jiang & Ruhai Yi

  6. Metabolic Diseases Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China

    Zhen Jiang & Ruhai Yi

  7. Department of Pathology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China

    Sheng Luo

  8. Department of Thyroid and Breast Surgery, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China

    Huihao Zhang

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  2. Sheng Luo
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Contributions

RY designed the experiments. SL, YL, and HZ performed the experiments. ZJ and RY analyzed the data. ZJ and RY prepared an initial draft of the manuscript. HZ and RY revised the manuscript. All the authors commented on and approved the final draft.

Corresponding authors

Correspondence to Huihao Zhang or Ruhai Yi.

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Jiang, Z., Luo, S., Lin, Y. et al. Correlations of m6A methylation-related mRNAs with thyroid cancer. Sci Rep (2026). https://doi.org/10.1038/s41598-026-35712-1

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  • Received: 07 May 2025

  • Accepted: 07 January 2026

  • Published: 19 January 2026

  • DOI: https://doi.org/10.1038/s41598-026-35712-1

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Keywords

  • Thyroid cancer
  • N6-methyladenosine
  • Pathway in cancer
  • RNA modification
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