Published September 16, 2015 | Version v1
Journal article

The Potential Role of Hedgehog Signaling in the Luminal/Basal Phenotype of Breast Epithelia and in Breast Cancer Invasion and Metastasis

  • 1. Department of Pathology, Faculty of Medicine, Umm Al-Qura University, Makkah 24382 (Saudi Arabia)
  • 2. Department of Biological, Biomedical and Analytical Sciences, Faculty of Health and Applied Sciences, University of West of England, Bristol BS16 1QY (United Kingdom)

Description

The epithelium of the lactiferous ducts in the breast is comprised of luminal epithelial cells and underlying basal myoepithelial cells. The regulation of cell fate and transit of cells between these two cell types remains poorly understood. This relationship becomes of greater importance when studying the subtypes of epithelial breast carcinoma, which are categorized according to their expression of luminal or basal markers. The epithelial mesenchymal transition (EMT) is a pivotal event in tumor invasion. It is important to understand mechanisms that regulate this process, which bears relation to the normal dynamic of epithelial/basal phenotype regulation in the mammary gland. Understanding this process could provide answers for the regulation of EMT in breast cancer, and thereby identify potential targets for therapy. Evidence points towards a role for hedgehog signaling in breast tissue homeostasis and also in mammary neoplasia. This review examines our current understanding of role of the hedgehog-signaling (Hh) pathway in breast epithelial cells both during breast development and homeostasis and to assess the potential misappropriation of Hh signals in breast neoplasia, cancer stem cells and tumor metastasis via EMT

Availability note (English)

Available from http://dx.doi.org/10.3390/cancers7030866; Available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586799

Additional details

Publishing Information

Journal Title
Cancers (Basel)
Journal Volume
7
Journal Issue
3
Journal Page Range
p. 1863-1884
ISSN
2072-6694

Optional Information

Copyright
Copyright (c) 2015 by the authors
Notes
PMCID: PMC4586799; PMID: 26389956; PUBLISHER-ID: cancers-07-00866; OAI: oai:pubmedcentral.nih.gov:4586799; licensee MDPI, Basel, Switzerland.; This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).