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Updated: Jan 13, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

IGF2BP2はm6A依存性STAT1 mRNA不安定化を介して甲状腺癌の脱分化を駆動する

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

Abstract:

Thyroid cancer is the most common endocrine malignancy globally. While papillary thyroid carcinoma (PTC) typically exhibits favorable prognosis, a subset undergoes dedifferentiation into anaplastic thyroid carcinoma (ATC), an aggressive, treatment-refractory subtype with near-universal lethality. However, the molecular driver of this process remains elusive. In this study, we find that IGF2BP2 is upregulated in ATC and correlates with adverse prognosis. Pseudotime trajectory analysis tracks progressively escalating IGF2BP2 expression throughout dedifferentiation. Functionally, IGF2BP2 promotes proliferation, suppresses thyroid differentiation genes (TSHR, SLC26A4, SLC5A5, TPO, PAX8, FOXE1, and NKX2.1), and enhances cancer stemness. Mechanistically, integrated multi-omics analysis (RNA-seq, RIP-seq, and MeRIP-seq) reveals that IGF2BP2 binds m6A-modified STAT1 mRNA, accelerating its decay. STAT1 directly activates transcription of thyroid differentiation genes. Rescue experiments confirms that STAT1 mediates IGF2BP2-driven dedifferentiation. The IGF2BP2-m6A-STAT1 complex is a master regulator of thyroid cancer dedifferentiation, establishing a novel therapeutic target for redifferentiation therapy in advanced thyroid cancer.

キーワード:

IGF2BP2 STAT1 m6A 幹性甲状腺癌の脱分化

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Induction and Analysis of Epithelial to Mesenchymal Transition

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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

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