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Insulin‐like growth factor‐I expression in normal and diseased endometrium
Author(s) -
Maiorano Eugenio,
Loverro Giuseppe,
Viale Giuseppe,
Giannini Teresa,
Napoli Anna,
Perlino Elda
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990118)80:2<188::aid-ijc5>3.0.co;2-e
Subject(s) - endocrinology , endometrium , growth factor , medicine , biology , insulin like growth factor , receptor , endometrial cancer , immunohistochemistry , neoplastic transformation , cancer research , cancer , carcinogenesis
While the role of steroid hormones in the regulation of endometrial proliferation and differentiation is well established, the effects of growth factors and their receptors in normal and neoplastic endometrium remain a matter of debate. Previous studies have documented the positive effects of insulin‐like growth factor‐I (IGF‐I) on epithelial cell proliferation and the active production of this growth factor in endometrial tissues. In view of decreased expression of transforming growth factor‐β1 (TGF‐β1), an antagonist of IGF‐I, in endometrial carcinoma, we investigated the expression of IGF‐I, at both the mRNA and protein levels, and the immunoreactivity for type I IGF‐I receptor in 30 formalin‐fixed, paraffin‐embedded tissue samples of normal and neoplastic endometrium, in order to possibly clarify the role of IGF‐I in endometrial proliferation and differentiation. Our results demonstrate a reduced expression of IGF‐I mRNA in endometrial carcinomas compared with non‐neoplastic tissues, despite equivalent immunohistochemical expression of IGF‐I and IGF‐I receptor. Our data suggest that IGF‐I and its corresponding receptor may not be directly involved in endometrial cancer cell proliferation and differentiation in vivo, though other components of the IGF‐I system ( e.g., IGF binding proteins) may affect endometrial malignant transformation and tumor progression. Int. J. Cancer 80:188–193, 1999. © 1999 Wiley‐Liss, Inc.