Cytotoxic and genotoxic effects of ¹³¹I and ⁶⁰Co in follicular thyroid cancer cell (WRO) with and without recombinant human thyroid‐stimulating hormone treatment

Abstract

Normally, differentiated thyroid cancer (DTC) tends to be biologically indolent, highly curable and has an excellent prognosis. However, the treatment may fail when the cancer has lost radioiodine avidity. The present study was carried out in order to evaluate the cytotoxic and genotoxic effects of I and Co and radioiodine uptake in WRO cells, derived from DTC, harboring the BRAF mutation. WRO cells showed a relatively slow cell cycle of 96.3 h with an unstable karyotype containing various double minutes. The genotoxicity assay (micronucleus test) showed a relative high radioresistance to I (0.07-3.70 MBq/mL), independent of treatment with recombinant human thyroid-stimulating hormone (rhTSH). For the cytotoxicity assay, WRO cells were also relatively resistant to Co (range: 0.2-8.3 Gy), but with a gradual decrease of viability as a function of time for higher doses (20 and 40 Gy, starting from the fifth to sixth day). For internal irradiation with I, WRO cells showed a decline in viability at radioactive concentration higher than 1.85 MBq/mL; this was even more effective at 3.70 MBq/mL, but only when preceded by rhTSH, in coincidence with the highest level of I uptake. These data show promising results, since the loss of the ability of thyroid cells to concentrate radioiodine is considered to be one of the main factors responsible for the failure of I therapy in patients with DTC. The use of tumor-derived cell lines as a model for in vivo tumor requires, however, further investigations and deep evaluation of the corresponding in vivo effects. Environ. Mol. Mutagen. 58:451-461, 2017. © 2017 Wiley Periodicals, Inc.

Poly (lactic-co-glycolic acid)-encapsulated iodine-131 nanoparticles fabricated with rhTSH induce apoptosis and immobilization of thyroid cancer cells

“…Thyroid cancer is a common malignancy of the endocrine organs with a gradual increase in morbidity (1), and has become the fifth leading cause of cancer worldwide (2). Generally, the vast majority (>90%) of thyroid cancers are differentiated thyroid cancers (DTCs), including papillary thyroid cancer (PTC) and follicular thyroid carcinoma (FTC) (2).…”

“…Generally, the vast majority (>90%) of thyroid cancers are differentiated thyroid cancers (DTCs), including papillary thyroid cancer (PTC) and follicular thyroid carcinoma (FTC) (2). DTC usually tends to be biologically indolent, highly curable, and has a favorable prognosis after thyroidectomy followed by internal radiotherapy using iodine-131 ( 131 I) to abolish thyroid cancer metastases and remnants (1,3,4). However, thyroid cancer such as FTC has a chance of developing into aggressive thyroid carcinoma (ATC) with metastatic propensity and resistance to radioiodine; that is, thyroid cancer will become indolent and endow a worse outcome when the thyroid cancer cells lose radioiodine avidity (1,2,5).…”

“…DTC usually tends to be biologically indolent, highly curable, and has a favorable prognosis after thyroidectomy followed by internal radiotherapy using iodine-131 ( 131 I) to abolish thyroid cancer metastases and remnants (1,3,4). However, thyroid cancer such as FTC has a chance of developing into aggressive thyroid carcinoma (ATC) with metastatic propensity and resistance to radioiodine; that is, thyroid cancer will become indolent and endow a worse outcome when the thyroid cancer cells lose radioiodine avidity (1,2,5). It is well known that the efficacy of internal radiotherapy relies on the ability of thyroid cancer cells to absorb and accumulate active iodide (1).…”

“…However, thyroid cancer such as FTC has a chance of developing into aggressive thyroid carcinoma (ATC) with metastatic propensity and resistance to radioiodine; that is, thyroid cancer will become indolent and endow a worse outcome when the thyroid cancer cells lose radioiodine avidity (1,2,5). It is well known that the efficacy of internal radiotherapy relies on the ability of thyroid cancer cells to absorb and accumulate active iodide (1). Hence, exploring methods for potentiating the recruitment of active iodide in thyroid cancer cells is a feasible therapeutic strategy for treating ATC with metastases and its remnants.…”