Regulation of CD97 protein in thyroid carcinoma

Citation
C. Hoang-vu et al., Regulation of CD97 protein in thyroid carcinoma, J CLIN END, 84(3), 1999, pp. 1104-1109
Citations number
20
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
84
Issue
3
Year of publication
1999
Pages
1104 - 1109
Database
ISI
SICI code
0021-972X(199903)84:3<1104:ROCPIT>2.0.ZU;2-R
Abstract
CD97 is a dimeric glycoprotein belonging to the secretin receptor superfami ly 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 ca rcinomas 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 c ould be found, whereas in differentiated thyroid carcinomas, CD97 expressio n 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. A pproximately 50% of FTC-133 cells expressed the CD97 protein under basal cu lture conditions. No differences were found in the number of CD97-positive cells after TSH, forskolin, and insulin treatment compared to control value s. Epidermal growth factor treatment led to an increase in CD97 immunostain ing (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 CD 97-positive cells from 50% to 30%. TSH, forskolin, phorbol 12-myristate 13- acetate, and insulin showed no effect after 72-h pretreatment with RA, wher eas epidermal growth factor treatment led to a slight increase in the numbe r of the CD97-positive cells (from 30% to 40%) compared to the control valu e. These data suggest that CD97 expression may play an important role in th e dedifferentiation of thyroid tumors, and RA might interfere with this pro cess in thyroid carcinoma by suppressing the dedifferentiation marker CD97.