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Differential Transcriptional and Protein Expression of Thyroid-Stimulating Hormone Receptor in Ovarian Carcinomas

医学 甲状腺 甲状腺癌 内科学 免疫组织化学 内分泌学 激素 信使核糖核酸 癌变 受体 癌症研究 癌症 生物 基因 生物化学
作者
Gyftaki Revekka,C Liacos,Politi Ekaterini,Liontos Michalis,Katerina Saltiki,Papageorgiou Theocharis,Nikolaos Thomakos,Haidopoulos Dimitrios,Rodolakis Alexandros,Alevizaki Maria,Bamias Aristotelis,Meletios Α. Dimopoulos
出处
期刊:International Journal of Gynecological Cancer [BMJ]
卷期号:24 (5): 851-856 被引量:11
标识
DOI:10.1097/igc.0000000000000139
摘要

Thyroid-stimulating hormone (TSH) regulates normal thyroid function by binding to its receptor (thyroid-stimulating hormone receptor -TSHR) that is expressed at the surface of thyroid cells. Recently, it has been demonstrated that TSHR is abundantly expressed in several tissues apart from the thyroid, among them the normal ovarian surface epithelium. The role of TSHR expression outside the thyroid is not completely understood. The current study examines possible alterations of TSHR expression in ovarian carcinomas and its implication in ovarian carcinogenesis.Quantitative real-time polymerase chain reaction and immunohistochemistry analysis of TSHR expression were performed in 34 ovarian carcinoma specimens and 10 normal ovarian tissues (controls).Significant reduction in TSHR messenger RNA (mRNA) expression was detected in ovarian carcinomas (mean [SD]: 0.518 [0.0934] vs normal, 49.4985 [89.1626]; P < 0.001, Mann-Whitney U test), whereas TSHR protein levels were significantly increased (percentage of positive cells: cancer, 73.55% [20.09%], vs normal, 54.54% [21.14%]; intensity: cancer, 2.52 [0.508], vs normal 1 [0]; P = 0.012, Mann-Whitney U test). No significant differences in TSHR mRNA were found according to history of thyroid disease.Our study describes for the first time alterations in TSHR expression both at mRNA and protein levels in ovarian carcinomas. The discrepancy between the decreased levels of the TSHR mRNA and the increased protein expression has already been described in thyroid carcinomas and might be due to alterations in its degradation by the ubiquitin system or other unknown mechanisms. Further analysis could elucidate the role of these findings in ovarian carcinogenesis.

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