Iodide excess induces apoptosis in thyroid cells
through a p53-independent mechanism involving oxidative stress.
Importantly, NIS gene expression levels were also detected to be very low in oncogene-transformed rat thyroid cell
models, indicating an inverse correlation between oncogene activation and NIS expression in thyroid cancer models (82).
It seems that overexpression of AKT1 is capable of promoting cell proliferation, sensitization to TSH, and inhibiting apoptosis, but it is not sufficient to transform thyroid cells
by itself (19,20).
Normal thyroid cells
express phosphodiesterase subtypes PDE4, PDE5, PDE7, and PDE8 .
The thyroid nodule refers to the thyroid cells
localized in the lesions caused by abnormal growth.
For example, in regions with severe selenium (Se) deficiency, a higher incidence of thyroiditis may be documented, due to a decreased activity of selenium-dependent glutathione peroxidase activity within thyroid cells
. Selenium-dependent enzymes are also key elements in the regulation of the immune system.
 showed autocrine IGF-1 production in papillary thyroid cancer cells and also demonstrated IGF-1 immunoreactivity in thyroid cell
(b) MiR-195 expression in normal thyroid cell
line Nthy-ori 3-1 and PTC cell lines K1 and BCPAP.
Furthermore, high BMI leads to hyperinsulinemia and IR that also contribute to increased thyroid cell
proliferation and goiter formation.
Fusco, "Thyroid cell
transformation requires the expression of the HMGA1 proteins," Oncogene, vol.
Excluding thyroid cell
damage, two factors determine Tg concentration in most clinical situations.
Papillary carcinoma forms 85-90% of thyroid cancers in iodide-sufficient countries,  while the remaining epithelial thyroid cell
tumours are mainly follicular carcinomas.