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Macrophage-derived interleukin-1beta promotes human breast cancer cell migration and lymphatic adhesion in vitro

Storr, Sarah J.; Safuan, Sabreena; Ahmad, Narmeen; El-Refaee, Mohammed; Jackson, Andrew M.; Martin, Stewart G.

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Authors

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SARAH STORR sarah.storr@nottingham.ac.uk
Assistant Professor

Sabreena Safuan

Narmeen Ahmad

Mohammed El-Refaee

STEWART MARTIN STEWART.MARTIN@NOTTINGHAM.AC.UK
Professor of Cancer and Radiation Biology



Abstract

Lymphovascular invasion (LVI), encompassing blood and lymphatic vessel invasion, is an important event in tumourigenesis. Macrophages within the tumour microenvironment are linked to the presence of LVI and angiogenesis. This study investigates the role of macrophage-derived, caspase-1 dependent interleukin-1beta (IL-1?) in an in vitro model of LVI.
IL-1? significantly augmented the adhesion and transmigration of breast cancer cell lines MCF7 and MDA-MB-231 across endothelial cell barriers. MDA-MB-231 and MCF7 showed a higher percentage of adhesion to lymphatic endothelial cells than blood endothelial cells following endothelial cell IL-1? stimulation (P

Citation

Storr, S. J., Safuan, S., Ahmad, N., El-Refaee, M., Jackson, A. M., & Martin, S. G. (2017). Macrophage-derived interleukin-1beta promotes human breast cancer cell migration and lymphatic adhesion in vitro. Cancer Immunology, Immunotherapy, 66(10), 1287-1294. https://doi.org/10.1007/s00262-017-2020-0

Journal Article Type Article
Acceptance Date May 20, 2017
Online Publication Date May 27, 2017
Publication Date 2017-10
Deposit Date May 25, 2017
Publicly Available Date May 27, 2017
Journal Cancer Immunology, Immunotherapy
Print ISSN 0340-7004
Electronic ISSN 1432-0851
Publisher Springer Verlag
Peer Reviewed Peer Reviewed
Volume 66
Issue 10
Pages 1287-1294
DOI https://doi.org/10.1007/s00262-017-2020-0
Keywords interleukin-1; breast cancer; macrophage; vascular invasion; caspase-1
Public URL https://nottingham-repository.worktribe.com/output/862235
Publisher URL https://link.springer.com/article/10.1007%2Fs00262-017-2020-0

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