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Gadd45B Deficiency Drives Radio-Resistance in BRAFsup.V600E-Mutated Differentiated Thyroid Cancer by Disrupting Iodine Metabolic Genes
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Gadd45B Deficiency Drives Radio-Resistance in BRAFsup.V600E-Mutated Differentiated Thyroid Cancer by Disrupting Iodine Metabolic Genes
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Gadd45B Deficiency Drives Radio-Resistance in BRAFsup.V600E-Mutated Differentiated Thyroid Cancer by Disrupting Iodine Metabolic Genes
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Journal Article
Gadd45B Deficiency Drives Radio-Resistance in BRAFsup.V600E-Mutated Differentiated Thyroid Cancer by Disrupting Iodine Metabolic Genes
2025
Overview
Radioactive iodine (RAI) is a cornerstone therapy for differentiated thyroid cancer, but many tumours—especially those with the BRAF[sup.V600E] mutation—become RAI-refractory and stop taking up iodine. We analysed patient tissues and public datasets and found that Gadd45B is consistently reduced in RAI-refractory disease. Using thyroid cancer cell lines and mouse models (including patient-derived xenografts), we show that restoring Gadd45B re-sensitises tumours to RAI, increases uptake, and slows growth. Mechanistically, Gadd45B modulates two complementary axes: it interacts with MAP3K4 to dampen MAPK signalling, and it restrains MYCBP–c-Myc–TERT activity. Together, these effects upregulate iodine-handling genes (e.g., NIS, TPO, Tg) and improve tumour differentiation. Clinically, low Gadd45B correlates with poor outcomes, supporting its potential as a biomarker and therapeutic target. While intratumoural recombinant Gadd45B showed benefit in vivo, we did not directly confirm its cellular entry; future studies will test delivery strategies and validate safety in patients.
Publisher
MDPI AG
