Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/104074
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Type: Journal article
Title: Interplay between CCR7 and Notch1 axes promotes stemness in MMTV-PyMT mammary cancer cells
Author: Boyle, S.
Gieniec, K.
Gregor, C.
Faulkner, J.
McColl, S.
Kochetkova, M.
Citation: Molecular Cancer, 2017; 16(1):19-1-19-8
Publisher: Biomed Central
Issue Date: 2017
ISSN: 1476-4598
1476-4598
Statement of
Responsibility: 
Sarah T. Boyle, Krystyna A. Gieniec, Carly E. Gregor, Jessica W. Faulkner, Shaun R. McColl and Marina Kochetkova
Abstract: Background: Breast cancer is the major cause of cancer-related mortality in women. It is thought that quiescent stem-like cells within solid tumors are responsible for cancer maintenance, progression and eventual metastasis. We recently reported that the chemokine receptor CCR7, a multi-functional regulator of breast cancer, maintains the stem-like cell population. Methods: This study used a combination of molecular and cellular assays on primary mammary tumor cells from the MMTV-PyMT transgenic mouse with or without CCR7 to examine the signaling crosstalk between CCR7 and Notch pathways. Results: We show for the first time that CCR7 functionally intersects with the Notch signaling pathway to regulate mammary cancer stem-like cells. In this cell subpopulation, CCR7 stimulation activated the Notch signaling pathway, and deletion of CCR7 significantly reduced the levels of activated cleaved Notch1. Moreover, blocking Notch activity prevented specific ligand-induced signaling of CCR7 and augmentation of mammary cancer stem-like cell function. Conclusion: Crosstalk between CCR7 and Notch1 promotes stemness in mammary cancer cells and may ultimately potentiate mammary tumor progression. Therefore, dual targeting of both the CCR7 receptor and Notch1 signaling axes may be a potential therapeutic avenue to specifically inhibit the functions of breast cancer stem cells.
Keywords: Breast cancer
CCR7
Cancer stem cell
Chemokine receptor
Crosstalk
Mammary gland
Notch
Rights: © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
DOI: 10.1186/s12943-017-0592-0
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