Association of the membrane estrogen receptor, GPR30, with breast tumor metastasis and transactivation of the epidermal growth factor receptor.

Full Abstract

The epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases function as a common signaling conduit for membrane receptors that lack intrinsic enzymatic activity, such as G-protein coupled receptors and integrins. GPR30, an orphan member of the seven transmembrane receptor (7TMR) superfamily has been linked to specific estrogen binding, rapid estrogen-mediated activation of adenylyl cyclase and the release of membrane-tethered proHB-EGF. More recently, GPR30 expression in primary breast adenocarcinoma has been associated with pathological parameters commonly used to assess breast cancer progression, including the development of extramammary metastases. This newly appreciated mechanism of cross communication between estrogen and EGF is consistent with the observation that 7TMR-mediated transactivation of the EGFR is a recurrent signaling paradigm and may explain prior data reporting the EGF-like effects of estrogen. The molecular details surrounding GPR30-mediated release of proHB-EGF, the involvement of integrin beta1 as a signaling intermediary in estrogen-dependent EGFR action, and the possible implications of these data for breast cancer progression are discussed herein.

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Author information

Author/s: Filardo, Edward J (EJ); Quinn, Jeffrey A (JA); Sabo, Edmond (E);

Affiliation: Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, RI 02903, USA. edward_filardo(-atsign-)brown.edu

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Review

Journal: Steroids (Steroids), published in United States. (Language: eng)

Reference: 2008-Oct; vol 73 (issue 9-10) : pp 870-3

Dates: Created 2008/06/06; Completed 2008/09/03;

PMID: 18289622, status: MEDLINE (last retrieval date: 11/6/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals
Breast Neoplasms - metabolism; pathology
Cell Communication
Cell Line, Tumor
Disease Progression
Estrogens - metabolism
Humans
Integrins - metabolism

Integrins - metabolism
Models, Biological
Neoplasm Metastasis
Neoplasms - pathology
Receptors, Estrogen - metabolism
Receptors, G-Protein-Coupled - metabolism
Signal Transduction
Trans-Activation (Genetics)

Associated Chemicals: Estrogens (0) ; GPER protein, human (0) ; Integrins (0) ; Receptors, Estrogen (0) ; Receptors, G-Protein-Coupled (0)

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