{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["22(4)"],"submitter":["Radom M"],"pubmed_abstract":["Radioiodine (RAI) therapy, used for treating differentiated thyroid cancers (DTCs), hinges on the functional expression of the sodium-iodide symporter (NIS). However, up to 60% of papillary thyroid carcinomas, the most common DTC subtype, harbor BRAF<sup>V600E</sup> mutations, which are strongly associated with reduced NIS expression, impaired RAI uptake, and poor differentiation scores. For patients with RAI-refractory, a promising therapeutic strategy is to restore RAI sensitivity by inducing tumor redifferentiation. Here, we demonstrate that NOX4-derived reactive oxygen species (ROS) contribute to NIS repression in BRAF<sup>V600E</sup>-mutated thyroid cancer cells. Particularly, NOX4-generated oxidative DNA damage recruits DNA repair proteins, including OGG1 and MSH2/MSH6 proteins, whic"],"journal":["International journal of biological sciences"],"pagination":["1674-1692"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12905579"],"repository":["biostudies-literature"],"pubmed_title":["NOX4-derived oxidative DNA damage impairs thyroid differentiation through an epigenetic mechanism in BRAF-mutated radioactive iodine refractory papillary thyroid cancer cells."],"pmcid":["PMC12905579"],"pubmed_authors":["Harinquet M","Buffet C","Bani MA","Droin N","Dayris T","Cazarin J","Ghuzlan AA","Braye F","Aglave M","Leboulleux S","Mesloub Y","Godefroy K","Dupuy C","de Faria CC","Radom M","Lamartina L","Nobre C"],"additional_accession":[]},"is_claimable":false,"name":"NOX4-derived oxidative DNA damage impairs thyroid differentiation through an epigenetic mechanism in BRAF-mutated radioactive iodine refractory papillary thyroid cancer cells.","description":"Radioiodine (RAI) therapy, used for treating differentiated thyroid cancers (DTCs), hinges on the functional expression of the sodium-iodide symporter (NIS). However, up to 60% of papillary thyroid carcinomas, the most common DTC subtype, harbor BRAF<sup>V600E</sup> mutations, which are strongly associated with reduced NIS expression, impaired RAI uptake, and poor differentiation scores. For patients with RAI-refractory, a promising therapeutic strategy is to restore RAI sensitivity by inducing tumor redifferentiation. Here, we demonstrate that NOX4-derived reactive oxygen species (ROS) contribute to NIS repression in BRAF<sup>V600E</sup>-mutated thyroid cancer cells. Particularly, NOX4-generated oxidative DNA damage recruits DNA repair proteins, including OGG1 and MSH2/MSH6 proteins, whic","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026","modification":"2026-07-15T16:32:03.852Z","creation":"2026-07-07T03:08:37.172Z"},"accession":"S-EPMC12905579","cross_references":{"pubmed":["41694580"],"doi":["10.7150/ijbs.123980"]}}