Xiang Jianjian, Lv Nannan, Yin Shanyu, Zhao Tong, Liu Fei, Cheng Lan, Liu Feng, Kuang Jinsong
Department of Ultrasound Medicine, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310000, China.
Department of Endocrinology, The Fourth People's Hospital of Shenyang, China Medical University, 20 Huanghe South Street, Huanggu District, Shenyang, 10032, China.
Thyroid Res. 2025 Jun 10;18(1):25. doi: 10.1186/s13044-025-00243-w.
Transforming growth factor-β (TGF-β) plays well-established roles in cancer cell invasion and epithelial-mesenchymal transition (EMT); however, its role in thyroid carcinoma (TC) remains unclear. This study aimed to evaluate the effects of TGF-β on EMT in TC and determine its underlying mechanisms.
Treatment of TC cell lines with TGF-β the morphology of thyroid cancer cells changed, Immunofluorescence staining revealed that the localization of E-cadherin shifted from the cell membrane to the cytoplasm, and the fluorescence intensity decreases. Wound-healing assay in BCPAP and TPC-1 revealed that migration ability was significantly higher in the TGF-β (5 ng/mL) treatment group than in the control group (P < 0.01).
Transwell assays showed that the invasive abilities of TGF-β-treated BCPAP, TPC-1, and K1 cells were 7-, 10-, and 6-fold higher than those of the control group, respectively (P < 0.05). After TGF-β treatment, mRNA levels of SNAI1 significantly increased in TPC-1 and BCPAP cell lines. Treatment of TC cell lines with TGF-β downregulated the epithelial marker E-cadherin and upregulated the mesenchymal markers N-cadherin and vimentin, at the mRNA level. Western blotting indicated similar results at the protein level, TSH could enhance this process.
TGF-β promotes EMT-like phenotypic changes in thyroid cancer cells, accompanied by upregulation of SNAI1 and EMT-related markers, which is enhanced by TSH. Overall, this study provides a basis for the development of therapeutic strategies for TC targeting the EMT.
转化生长因子-β（TGF-β）在癌细胞侵袭和上皮-间质转化（EMT）中发挥着既定作用；然而，其在甲状腺癌（TC）中的作用仍不清楚。本研究旨在评估TGF-β对TC中EMT的影响并确定其潜在机制。
用TGF-β处理TC细胞系后，甲状腺癌细胞的形态发生改变，免疫荧光染色显示E-钙黏蛋白的定位从细胞膜转移至细胞质，且荧光强度降低。BCPAP和TPC-1细胞的伤口愈合试验显示，TGF-β（5 ng/mL）处理组的迁移能力显著高于对照组（P < 0.01）。
Transwell试验表明，TGF-β处理的BCPAP、TPC-1和K1细胞的侵袭能力分别比对照组高7倍、10倍和6倍（P < 0.05）。TGF-β处理后，TPC-1和BCPAP细胞系中SNAI1的mRNA水平显著升高。在mRNA水平上，用TGF-β处理TC细胞系可下调上皮标志物E-钙黏蛋白并上调间质标志物N-钙黏蛋白和波形蛋白。蛋白质印迹在蛋白质水平上显示了类似结果，促甲状腺激素（TSH）可增强这一过程。
TGF-β促进甲状腺癌细胞发生EMT样表型变化，同时伴有SNAI1和EMT相关标志物的上调，TSH可增强这种作用。总体而言，本研究为针对EMT的TC治疗策略的开发提供了依据。
