Thyroid-stimulating hormone receptor affects metastasis and prognosis in papillary thyroid carcinoma

T.-R. Liu, X. Su, W.-S. Qiu, W.-C. Chen, Q.-Q. Men, L. Zou, Z.-Q. Li, X.-Y. Fu, A.-K. Yang

Department of Otorhinolaryngology Head and Neck Surgery, The Sixth Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China. yangak@sysucc.org.cn

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• Oncology

OBJECTIVE: Although endocrine therapy of papillary thyroid carcinoma (PTC) by inhibiting thyroid-stimulating hormone (TSH) has been used for many years, its mechanism of action is not clear. This study aimed to explore the expression and role of TSH receptor (TSHR) in PTC, to provide a theoretical basis for optimization of endocrine treatment options in PTC.

PATIENTS AND METHODS: Expression of TSHR was tested by immunohistochemistry of tissues from 150 cases of PTC and 21 normal thyroid tissues. Survival analysis was performed by Kaplan-Meier and log-rank analyses, and multivariate analysis was done using a Cox model. The regulatory effects of the TSH-TSHR signal transduction pathway on differentiated thyroid carcinoma cells were explored in vitro.

RESULTS: The positive expression rate of TSHR in PTC was 68% (102/150). TSHR expression was an independent factor affecting the prognosis of PTC patients aged > 45 years (p = 0.006), and TSHR might have a role in decreasing distant metastasis (p = 0.024). In vitro experiments showed that up-regulation of TSHR promoted apoptosis of thyroid cancer cells and inhibited metastasis significantly. There was no significant regulatory effect of the TSH-TSHR signal transduction pathway on the proliferation of thyroid carcinoma cells.

CONCLUSIONS: TSHR expression is an independent factor that affects the prognosis of PTC patients, and might decrease distant metastasis in patient aged > 45 years. Up-regulation of TSHR could inhibit metastasis and promote apoptosis in PTC cells.

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