Hoang-Vu C, Bull K, Schwarz I, Krause G, Schmutzler C, Aust G, Köhrle J, Dralle H
Klinik für Allgemeinchirurgie, Martin Luther Universität Halle-Wittenberg, Halle, Germany.
J Clin Endocrinol Metab. 1999 Mar;84(3):1104-9. doi: 10.1210/jcem.84.3.5557.
CD97 is a dimeric glycoprotein belonging to the secretin receptor superfamily and is abundantly expressed in cells of hematopoietic origin. The aim of this study was to analyze the expression of the CD97 protein in thyroid carcinomas and the role of all-trans-retinoic acid (RA) in the regulation of CD97 protein in monolayer culture of the human follicular thyroid carcinoma cell line FTC-133. In normal thyroid tissue, no immunoreactivity of CD97 could be found, whereas in differentiated thyroid carcinomas, CD97 expression was either lacking or low. Undifferentiated anaplastic thyroid carcinomas revealed high CD97 expression. The expression of CD97 protein seems to be correlated to the postoperative histopathological classification staging. Approximately 50% of FTC-133 cells expressed the CD97 protein under basal culture conditions. No differences were found in the number of CD97-positive cells after TSH, forskolin, and insulin treatment compared to control values. Epidermal growth factor treatment led to an increase in CD97 immunostaining (up to 90%), whereas phorbol 12-myristate 13-acetate slightly decreased the immunoreactivity of CD97 (from 50% to 30%). Under basal conditions, RA treatment for 72 h led to a decrease in total cell number by 33% and in CD97-positive cells from 50% to 30%. TSH, forskolin, phorbol 12-myristate 13-acetate, and insulin showed no effect after 72-h pretreatment with RA, whereas epidermal growth factor treatment led to a slight increase in the number of the CD97-positive cells (from 30% to 40%) compared to the control value. These data suggest that CD97 expression may play an important role in the dedifferentiation of thyroid tumors, and RA might interfere with this process in thyroid carcinoma by suppressing the dedifferentiation marker CD97.
CD97是一种二聚体糖蛋白，属于促胰液素受体超家族，在造血来源的细胞中大量表达。本研究的目的是分析CD97蛋白在甲状腺癌中的表达以及全反式维甲酸（RA）在人甲状腺滤泡癌细胞系FTC - 133单层培养中对CD97蛋白的调控作用。在正常甲状腺组织中，未发现CD97的免疫反应性，而在分化型甲状腺癌中，CD97表达缺失或较低。未分化的间变性甲状腺癌显示出高CD97表达。CD97蛋白的表达似乎与术后组织病理学分类分期相关。在基础培养条件下，约50%的FTC - 133细胞表达CD97蛋白。与对照值相比，促甲状腺激素（TSH）、福斯高林和胰岛素处理后，CD97阳性细胞数量未发现差异。表皮生长因子处理导致CD97免疫染色增加（高达90%），而佛波酯12 - 肉豆蔻酸13 - 乙酸酯略微降低了CD97的免疫反应性（从50%降至30%）。在基础条件下，RA处理72小时导致总细胞数减少33%，CD97阳性细胞从50%降至30%。用RA预处理72小时后，TSH、福斯高林、佛波酯12 - 肉豆蔻酸13 - 乙酸酯和胰岛素均无作用，而与对照值相比，表皮生长因子处理导致CD97阳性细胞数量略有增加（从30%增至40%）。这些数据表明，CD97表达可能在甲状腺肿瘤的去分化中起重要作用，并且RA可能通过抑制去分化标志物CD97来干扰甲状腺癌中的这一过程。
