Journal article

Ghrelin and des-acyl ghrelin inhibit aromatase expression and activity in human adipose stromal cells: suppression of cAMP as a possible mechanism

Maria M Docanto, Fangyuan Yang, Brid Callaghan, CheukMan C Au, Rahini Ragavan, Xuyi Wang, John B Furness, Zane B Andrews, Kristy A Brown

BREAST CANCER RESEARCH AND TREATMENT | SPRINGER | Published : 2014

Abstract

Aromatase converts androgens into estrogens and its expression within adipose stromal cells (ASCs) is believed to be the major driver of estrogen-dependent cancers in older women. Ghrelin is a gut-hormone that is involved in the regulation of appetite and known to bind to and activate the cognate ghrelin receptor, GHSR1a. The unacylated form of ghrelin, des-acyl ghrelin, binds weakly to GHSR1a but has been shown to play an important role in regulating a number of physiological processes. The aim of this study was to determine the effect of ghrelin and des-acyl ghrelin on aromatase in primary human ASCs. Primary human ASCs were isolated from adipose tissue of women undergoing cosmetic surgery..

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University of Melbourne Researchers

Grants

Awarded by NHMRC (Australia)


Awarded by National Breast Cancer Foundation


Funding Acknowledgements

This research was supported by NHMRC (Australia) Project Grant # GNT1005735 and by a grant from the National Breast Cancer Foundation (NC-14-011) to KAB, and by the Victorian Government Operational Infrastructure Support Program. KAB is supported by an NHMRC (Australia) Career Development Award GNT1007714. We thank Mr Seungmin Ham for his technical support.