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Expression of activin and inhibin subunits, receptors and binding proteins in Human adrenocortical neoplasms
Author(s) -
Hofland J.,
Timmerman M. A.,
De Herder W. W.,
Van Schaik R. H. N.,
De Krijger R. R.,
De Jong F. H.
Publication year - 2006
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.2006.02668.x
Subject(s) - follistatin , activin receptor , endocrinology , medicine , adrenocortical carcinoma , receptor , activin type 2 receptors , biology , adrenal cortex , protein subunit , acvr2b , messenger rna , gene expression , carcinogenesis , gene , tgf beta signaling pathway , cancer , biochemistry
Summary Objective The growth and differentiation factors activin and inhibin can affect tumour formation and steroid production in the adrenal cortex. These factors bind to type I (Alk‐4), type II (ActRIIA, ActRIIB) and type III (betaglycan) receptors or to the activin‐binding protein follistatin. Expression of these activin‐related mRNAs was measured in different types of adrenocortical tissues and tumours to study the relationship with tumorigenesis. Design Quantitative expression of activin‐related mRNAs was investigated in patient adrenocortical samples. Patients Twenty‐eight human adrenocortical samples from normal and hyperplastic adrenals and from adrenocortical adenomas and carcinomas were collected after surgery for study purposes. Measurements Using quantitative reverse transcription polymerase chain reaction (RT‐PCR), we investigated the expression of inhibin α‐, βA‐ and βB‐subunits, follistatin, betaglycan, ActRIIA, ActRIIB and Alk‐4 in the adrenocortical tissues. The expression of cytochrome P450c17 (CYP17) mRNA was also measured to investigate its association with inhibin and activin subunit expression. Results All genes studied were expressed in all tissues, with the exception of the inhibin α‐subunit in one hyperplastic adrenal and three adrenocortical carcinomas. Expression of inhibin βA‐subunit, follistatin, betaglycan, ActRIIA, ActRIIB and CYP17 differed between nontumorous adrenals and carcinomas. Conclusions These differences, together with correlation analysis, indicate parallel regulation of the expression of CYP17, the inhibin α‐subunit, ActRIIA, ActRIIB, betaglycan and follistatin. We conclude that the expression of activin and inhibin subunits, receptors and binding proteins is affected by tumour formation in the adrenal gland and may play a role in tumorigenesis.