Skip to main content
padlock icon - secure page this page is secure

Expression of adrenocorticotrophic hormone receptor mRNA in human adrenocortical neoplasms: correlation with P450scc expression

Buy Article:

$52.00 + tax (Refund Policy)

OBJECTIVEAdrenocorticotrophin (ACTH) is the main hormone-regulating steroid secretion from the adrenal cortex. The ACTH receptor (ACTH-R) has recently been cloned, allowing systematic evaluation of its expression and function in adrenal tumorigenesis. We investigated ACTH-R and P450 side-chain cleavage enzyme (P450scc) mRNA expression in a variety of neoplastic adrenocortical tissues by Northern blot and reverse-transcriptase-PCR (RT-PCR).

PATIENTS AND MEASUREMENTSWe studied tissue from eight normal adrenals, six diffuse adrenocortical hyperplasias in patients with ACTH-dependent Cushing's syndrome, 22 adrenal adenomas, six carcinomas and two carcinoma cell lines. Poly A mRNA was electrophoresed, immobilized on a nylon membrane and hybridized using α32P-CTP labelled human ACTH-R and P450scc cDNAs.

RESULTSMean ACTH-R mRNA expression showed significant differences between groups (P=0.0001), but appeared to be independent of plasma ACTH concentrations. Compared to normal adrenal =100±12%), expression was low in non-functional adenomas (23±11%) and carcinomas (19±12%), intermediate in adrenocortical hyperplasias (88±6%) and cortisol-producing adenomas (81±15%) and high in aldosteronomas (175±29%). In adenomas, ACTH-R mRNA expression correlated closely with the expression of P450scc mRNA r=0.8, P=0.0001) suggesting regulation by similar factors. However, carcinomas and cancer cell lines did not show a positive correlation between these two parameters r=−0.44, P=0.2).

CONCLUSIONSWe have demonstrated that plasma ACTH is not the major factor influencing ACTH-receptor mRNA expression in neoplastic adrenal tissue. In benign tumours of the adrenal cortex there was a close positive correlation between ACTH-receptor mRNA and P450scc mRNA which was missing in adrenocortical carcinomas, probably as a result of tumour dedifferentiation.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Document Type: Research Article

Affiliations: 1: Department of Internal Medicine, University of Würzburg, FRG, 2: Developmental Endocrinology Branch, NICHD, National Institutes of Health, Bethesda, MD, USA

Publication date: May 1, 1997

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more