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In situ analysis of transforming growth factors‐β(TGF‐β1, TGG‐β2, TGF‐β3) and TGF–β type II receptor expression in basal cell carcinomas
Author(s) -
SCHMID P.,
ITIN P.,
RUFLI TH.
Publication year - 1996
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1996.d01-899.x
Subject(s) - paracrine signalling , transforming growth factor , biology , in situ hybridization , stromal cell , tgf alpha , stroma , hair follicle , transforming growth factor beta , epidermis (zoology) , pathology , messenger rna , cancer research , receptor , growth factor , immunohistochemistry , endocrinology , immunology , medicine , gene , anatomy , biochemistry
Summary Transforming growth factor‐beta (TGF‐β) consists of a highly homologous family of multifunctional peptides which are differentially expressed and function in a wide range of target cells. Aberrant expressions of TGFβs have been implicated in a number of disease processes, particularly those involving fibrotic and inflammatory lesions, and loss of TGF‐β growth inhibition may play a part in the progression of certain neoplasms. In the present study, we have analysed and compared, by in situ hybridization, mRNA expression of transforming growth factors‐β(TGF‐β1, TGF‐β2. TGF‐β3) and TGF‐β type II receptor (TβR II). and. by immunohistochemistry, the distribution of TGF‐β3 protein in normal human skin and in basal cell carcinoma (BCC). The stroma of most BCCs revealed enhanced TGF‐β1 and TβR II mRNA expression when compared with normal dermis. A minority of BCCs also showed stromal overexpression of TGF‐β2 and/or TGF‐β3 mRNA. However, tumour tissues of all BCCs revealed weaker TGF‐β3 mRNA and protein expression than normal interfollicular epidermis and hair follicle epithelia, whereas expression of TGF‐β1 mRNA was comparably weak in tumour tissues and normal skin epithelia. Expression of TGF‐β2 mRNA, which was clearly detectable in distinct hair follicle epithelia, was only barely detectable in normal interfollicular epidermis and in tumour tissues. In contrast, abundant TβR II mRNA expression was observed both in normal skin epithelia and tumour tissues. From these findings, we suggest that increased stromal TGF‐β activity induces fibrotic alterations which promote tumour survival and/or progression via paracrine mechanisms, whereas lack of TGF‐β expression by tumour cells may contribute to an autocrine growth control defect in BCCs.