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Involvement of early growth response factors in TNFα-induced aromatase expression in breast adipose.

Abstract：

:Expression of the oestrogen producing enzyme, aromatase, is regulated in a tissue-specific manner by its encoding gene CYP19A1. In post-menopausal women, the major site for oestrogen production in the breast is the adipose, where CYP19A1 transcription is driven by the distal promoter I.4 (PI.4). Transcripts via this promoter are also elevated in breast adipose fibroblasts (BAFs) adjacent to a tumour. PI.4 expression is stimulated by a number of cytokines, and TNFα is one such factor. The transcriptional mechanisms induced by TNFα to stimulate PI.4 are poorly characterised. We show that the early growth response (Egr) transcription factors play an important role in the TNFα-induced signalling pathway resulting in elevated PI.4 transcription. TNFα treatment of BAFs increases mRNA levels of all four Egr family members, with EGR2 being the most highly expressed. Overexpression of EGR2 causes an increase in endogenous CYP19A1 expression in preadipocyte Simpson-Golabi-Behmel syndrome cells, driven by increases in PI.4-specific transcripts. PI.4 luciferase reporter activity is increased in a dose-dependent manner by EGR2, EGR3 and EGR4, with EGR2 showing the most potent activation of promoter activity. Deletion analysis indicates that this promoter activity is being indirectly mediated by a short region of the promoter not containing any previously characterised binding sites, and we further show that EGR2 does not bind directly or indirectly to this promoter region. However, siRNA knockdown of the Egrs reduces the total and PI.4-derived CYP19A1 transcription in BAFs. These studies unveil a novel component of the aromatase gene regulatory network and further enhance the complexity of oestrogen production in the breast.

journal_name

Breast Cancer Res Treat

journal_title

Breast cancer research and treatment

authors

To SQ,Simpson ER,Knower KC,Clyne CD

doi

10.1007/s10549-013-2413-5

subject

Has Abstract

pub_date

2013-02-01 00:00:00

pages

193-203

issue

1

eissn

0167-6806

issn

1573-7217

journal_volume

138

pub_type

杂志文章

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