Affiliations 

  • 1 Division of Cancer and Stem Cells, Translational and Radiation Biology Research Group, School of Medicine, Academic Clinical Oncology, University of Nottingham, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, NG5 1PB, UK
  • 2 Division of Cancer and Stem Cells, Host-Tumour Interactions Group, School of Medicine, Academic Clinical Oncology, University of Nottingham, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, NG5 1PB, UK
  • 3 Division of Cancer and Stem Cells, Translational and Radiation Biology Research Group, School of Medicine, Academic Clinical Oncology, University of Nottingham, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, NG5 1PB, UK. stewart.martin@nottingham.ac.uk
Cancer Immunol Immunother, 2017 Oct;66(10):1287-1294.
PMID: 28551814 DOI: 10.1007/s00262-017-2020-0

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-1β) in an in vitro model of LVI. IL-1β 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-1β stimulation (P 

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.