Linking loss of sodium-iodide symporter expression to DNA damage
| Autor: | Therese Carlsson, Jan-Olof Karlsson, Ola Hammarsten, Jakob Himmelman, Per Postgård, Nirmal Kapoor, Mikael Nilsson, Madeleine Nordén Lyckesvärd, Camilla Ingeson-Carlsson, Eva Forssell-Aronsson |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Sodium-iodide symporter medicine.medical_specialty DNA damage Cell Survival Iodide Sus scrofa Thyroid Gland Thyrotropin Ataxia Telangiectasia Mutated Proteins Biology Epithelium 03 medical and health sciences Electrolytes Internal medicine medicine Animals Iodide transport Insulin-Like Growth Factor I health care economics and organizations Cells Cultured Cell Proliferation chemistry.chemical_classification Symporters Cell growth Kinase Thyroid Biological Transport Cell Biology Iodides Molecular biology 030104 developmental biology medicine.anatomical_structure Endocrinology Aminoglycosides chemistry Symporter DNA Damage |
| Zdroj: | Experimental cell research. 344(1) |
| ISSN: | 1090-2422 |
| Popis: | Radiotherapy of thyroid cancer with I-131 is abrogated by inherent loss of radioiodine uptake due to loss of sodium iodide symporter (NIS) expression in poorly differentiated tumor cells. It is also known that ionizing radiation per se down-regulates NIS (the stunning effect), but the mechanism is unknown. Here we investigated whether loss of NIS-mediated iodide transport may be elicited by DNA damage. Calicheamicin, a fungal toxin that specifically cleaves double-stranded DNA, induced a full scale DNA damage response mediated by the ataxia-telangiectasia mutated (ATM) kinase in quiescent normal thyrocytes. At sublethal concentrations ( |
| Databáze: | OpenAIRE |
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