Thyrotropin (TSH) suppression is required in the management of patients with papillary thyroid carcinoma (PTC) to improve their outcomes, inevitably causing iatrogenic thyrotoxicosis. Nevertheless, the evidence supporting this practice remains limited and weak, and in vitro studies examining the mitogenic effects of TSH in cancerous cells used supraphysiological doses of bovine TSH, which produced conflicting results. Our study explores, for the first time, the impact of human recombinant thyrotropin (rh-TSH) on human PTC cell lines (K1 and TPC-1) that were transformed to overexpress the thyrotropin receptor (TSHR). The cells were treated with escalating doses of rh-TSH under various conditions, such as the presence or absence of insulin. The expression levels ofTSHRandthyroglobulin(Tg) were determined, and subsequently, the proliferation and migration of both transformed and non-transformed cells were assessed. Under the conditions employed, rh-TSH was not adequate to induce either the proliferation or the migration rate of the cells, whileTgexpression was increased. Our experiments indicate that clinically relevant concentrations of rh-TSH cannot induce proliferation and migration in PTC cell lines, even after the overexpression of TSHR. Further research is warranted to dissect the underlying molecular mechanisms, and these results could translate into better management of treatment for PTC patients.
在甲状腺乳头状癌（PTC）患者的治疗中，通常需要抑制促甲状腺激素（TSH）以改善预后，但这不可避免地会导致医源性甲状腺毒症。然而，支持这一做法的证据仍然有限且薄弱，且现有体外研究在探讨TSH对癌细胞的促有丝分裂效应时，多使用超生理剂量的牛TSH，其结果存在矛盾。本研究首次探讨了人重组促甲状腺激素（rh-TSH）对过表达促甲状腺激素受体（TSHR）的人PTC细胞系（K1和TPC-1）的影响。研究在不同条件下（如存在或不存在胰岛素）使用递增剂量的rh-TSH处理细胞，检测了TSHR和甲状腺球蛋白（Tg）的表达水平，并进一步评估了转染细胞与未转染细胞的增殖和迁移能力。在实验条件下，rh-TSH未能有效诱导细胞增殖或迁移，但Tg表达有所增加。实验结果表明，即使TSHR过表达，临床相关浓度的rh-TSH仍无法诱导PTC细胞系的增殖和迁移。未来需进一步研究其潜在分子机制，这些结果可能为优化PTC患者的治疗方案提供依据。
肿瘤(癌症)患者之家