Amifostine does not protect thyroid cancer cells in DNA damaging in vitro models
| Autor: | Leonard Wartofsky, Aneeta Patel, Vasyl Vasko, Kenneth D. Burman, Joanna Klubo-Gwiezdzinska, Douglas Van Nostrand, Kirk Jensen, John Costello, Rok Tkavc |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
DNA damage Endocrinology Diabetes and Metabolism lcsh:Diseases of the endocrine glands. Clinical endocrinology 03 medical and health sciences 0302 clinical medicine Endocrinology thyroid cancer Internal Medicine medicine Cytotoxic T cell Viability assay amifostine Thyroid cancer chemistry.chemical_classification Reactive oxygen species lcsh:RC648-665 business.industry Research Amifostine medicine.disease In vitro radiation 030104 developmental biology chemistry Apoptosis 030220 oncology & carcinogenesis Cancer research business medicine.drug |
| Zdroj: | Endocrine Connections, Vol 6, Iss 7, Pp 469-478 (2017) Endocrine Connections |
| ISSN: | 2049-3614 |
| DOI: | 10.1530/ec-17-0138 |
| Popis: | Background Amifostine is a potent scavenger of reactive oxygen species that is used for the salivary gland protection during therapy with radioactive iodine for thyroid cancer. There are no data on the potential effect of amifostine on thyroid cancer cells. Methods We investigated the effects of the active form of amifostine (WR-1065) on the response of thyroid cancer cells to treatment with DNA-damaging agents. WR-1065 was examined in human thyroid cancer cell lines (FTC133, TPC1, BCPAP and C643) and embryonic fibroblast cells NIH3T3. DNA damage was induced by exposure to H2O2 (0.1 mM), by treatment with the radiomimetic neocarzinostatin (NCS 250 ng/mL) and by γ-radiation (6 Gy). DNA damage, cell viability and apoptosis were examined. Results We demonstrated the selective action of WR-1065 (0.1 mM), which prevented oxidative stress–induced DNA damage in fibroblasts, but did not protect thyroid cancer cells from DNA damage and apoptosis documented by caspase-3 and PARP cleavage after exposure to H2O2, NCS and γ-radiation. Prolonged exposure to WR-1065 (0.1 mM for 24 h) was toxic for thyroid cancer cells; this treatment decreased the number of viable cells by 8% in C643 cells, 47% in TPC cells, 92% in BCPAP cells and 82% in FTC 133 cells. The cytotoxic effects of WR-1065 were not associated with induction of apoptosis. Conclusions Our data show that amifostine has no protective effect on thyroid cancer cells against DNA-damaging agents in vitro and suggest that amifostine will not attenuate the efficacy of radioiodine treatment in patients with thyroid cancer. |
| Databáze: | OpenAIRE |
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