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Macrophage AEBP1 contributes to mammary epithelial cell hyperplasia as a novel regulator of sonic hedgehod signalling

Author: Ryan W Holloway; Dalhousie University. Department of Biochemistry & Moleculer Biology,
Publisher: Halifax, NS : Dalhousie University, 2012. ©2012 .
Dissertation: Thesis DEGREE Dalhousie University, 2013.
Edition/Format:   Thesis/dissertation : Document : Thesis/dissertation   Computer File : English
Summary:
ABSTRACT: Chronic inflammation stimulates mammary tumourigenesis by disrupting signalling interactions between the epithelial ducts and the surrounding stromal microenvironment. Adipocyte enhancer-binding protein 1 (AEBP1) promotes mammary epithelial cell hyperplasia as a stromal factor that enhances activity of the proinflammatory transcription factor Nuclear Factor-?B (NF-?B) in macrophages. Aberrant NF-?B  Read more...
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Details

Material Type: Document, Thesis/dissertation, Internet resource
Document Type: Book, Computer File, Internet Resource
All Authors / Contributors: Ryan W Holloway; Dalhousie University. Department of Biochemistry & Moleculer Biology,
OCLC Number: 936358237
Notes: Title from PDF title page (viewed Feb. 01, 2016).
Thesis supervisor: Hyo-Sung Ro
Description: 1 online resource (xv, 86 leaves) : illustrations.
Responsibility: by Ryan W. Holloway.

Abstract:

ABSTRACT: Chronic inflammation stimulates mammary tumourigenesis by disrupting signalling interactions between the epithelial ducts and the surrounding stromal microenvironment. Adipocyte enhancer-binding protein 1 (AEBP1) promotes mammary epithelial cell hyperplasia as a stromal factor that enhances activity of the proinflammatory transcription factor Nuclear Factor-?B (NF-?B) in macrophages. Aberrant NF-?B activity in macrophages elevates production of proinflammatory signals and the ligand sonic hedgehog (Shh), a significant contributor to tumourigenesis. In this study, Shh expression was elevated in macrophages isolated from transgenic mice (AEBP1TG) that overexpress AEBP1. Transient overexpression of AEBP1 in a macrophage cell line resulted in increased Shh expression. Furthermore, hedgehog target genes Gli1 and Bmi1 were up-regulated in mammary epithelium of AEBP1TG mice and HC11 mammary epithelial cells co-cultured with AEBP1TG macrophages. Growth of HC11 cells and mammary tumours was enhanced in response to AEBP1TG macrophages. These findings suggest that macrophage AEBP1 overexpression contributes to mammary hyperplasia through enhanced hedgehog signalling.

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