Oestrogen mediates the growth of human thyroid carcinoma cells via an oestrogen receptor – ERK pathway

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Abstract
Abstract.  Objectives: Although thyroid cancer occurs much more frequently in females, the role of sex hormones in thyroid carcinogenesis is unknown. In this study, it has been investigated how 17β‐oestradiol (E2) influenced proliferation and growth of thyroid cancer cells. Materials and Methods: Cell proliferation and its related molecules were examined in thyroid papillary carcinoma cells (KAT5), follicular thyroid carcinoma cells (FRO) and anaplastic carcinoma cells (ARO). Levels of oestrogen receptor (ER) α and β were regulated by their agonists (PPT and DPN), antagonists and siRNA. Results: E2 promoted cell proliferation. Such an effect was positively related to ERα but negatively to ERβ; PPT enhanced cell proliferation while DPN inhibited it. PPT increased Bcl‐2 expression while DPN decreased it. DPN also elevated Bax expression. PPT elevated the level of phosphorylated extracellular signal‐regulated kinase 1/2 (pERK1/2), suggesting a positive role of ERK1/2 in E2‐induced cell proliferation. Knockdown of ERα significantly attenuated E2‐mediated Bcl‐2 and pERK1/2 expression. In contrast, knockdown of ERβ markedly enhanced them. Conclusions: Oestrogen stimulates proliferation of thyroid cancer cells, associated with increase in Bcl‐2 and decrease in Bax levels in an ERK1/2‐related pathway. Imbalance between ERα and ERβ may contribute to thyroid carcinogenesis.

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