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IGF2BP2 Drives Thyroid Cancer Dedifferentiation Through m6A-Dependent STAT1 mRNA Destabilization
Rui Chen1, Yi-Xun Li1, Wei-Lin Lu1
1Department of Breast Surgery, the First Affiliated Hospital with Nanjing Medical University, 300 Guangzhou Road, 210029, Nanjing, People's Republic of China.
International Journal of Biological Sciences
|January 12, 2026
Summary
IGF2BP2 drives thyroid cancer dedifferentiation by targeting STAT1 mRNA, leading to aggressive anaplastic thyroid carcinoma (ATC). This discovery offers a new therapeutic target for redifferentiation therapy in advanced thyroid cancer.
Area of Science:
- Endocrinology
- Oncology
- Molecular Biology
Background:
- Thyroid cancer is a common endocrine malignancy.
- Anaplastic thyroid carcinoma (ATC) is an aggressive, lethal subtype arising from dedifferentiated papillary thyroid carcinoma (PTC).
- The molecular mechanisms driving PTC dedifferentiation to ATC remain largely unknown.
Purpose of the Study:
- To identify the molecular drivers of thyroid cancer dedifferentiation.
- To elucidate the mechanism by which these drivers promote aggressive tumor phenotypes.
- To establish a potential therapeutic target for advanced thyroid cancer.
Main Methods:
- Pseudotime trajectory analysis of gene expression.
- Functional assays assessing cell proliferation, differentiation, and cancer stemness.
- Integrated multi-omics analysis including RNA-seq, RIP-seq, and MeRIP-seq.
- Rescue experiments to validate mechanistic findings.
Main Results:
- IGF2BP2 is upregulated in ATC and correlates with poor prognosis.
- IGF2BP2 promotes proliferation, enhances cancer stemness, and suppresses thyroid differentiation genes.
- IGF2BP2 binds to m6A-modified STAT1 mRNA, promoting its degradation.
- STAT1 is essential for IGF2BP2-mediated thyroid cancer dedifferentiation.
Conclusions:
- The IGF2BP2-m6A-STAT1 complex is a key regulator of thyroid cancer dedifferentiation.
- Targeting this complex represents a novel therapeutic strategy for redifferentiation therapy in advanced thyroid cancer.
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