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E‐selectin‐mediated dynamic interactions of breast‐and colon‐cancer cells with endothelial‐cell monolayers
Author(s) -
Tözeren Aydin,
Kleinman Hynda K.,
Grant Derrick S.,
Morales David,
Mercurio Arthur M.,
Byers Stephen W.
Publication year - 1995
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910600326
Subject(s) - endothelial stem cell , breast carcinoma , e selectin , cancer research , umbilical vein , cell adhesion , pathology , medicine , cell , biology , immunology , endocrinology , breast cancer , in vitro , cancer , biochemistry
The molecular mechanisms involved in the dynamic interaction of human breast carcinoma cells with the endothelial cell lining of lymphatic vessels and post‐capillary blood venules are largely unknown. In the present study, laminar flow assays were used to investigate the ability of various normal breast cells and of breast‐ and colon‐tumor cells to adhere to human umbilical cord endothelial cell monolayers. MCF‐10A breast, MCF‐7 and T‐47D breast‐carcinoma and clone A, RKO, and HT‐29 colon‐carcinoma cells accumulated and rolled, in the presence of flow, on tumor necrosis factor (TNF)‐stimulated but not on unstimulated endothelial cell monolayers. Non‐tumor and tumor cells continued to form transient adhesions with TNF‐stimulated endothelial cells even when the flow rate was increased to levels found in arteries. Incubation of TNF‐stimulated endothelial cells with an E‐selectin‐specific monoclonal antibody (MAb) partially or completely inhibited dynamic interactions and diminished adhesion strength, whereas integrin β 1 ‐ and integrin α 6 ‐specific MAbs had no effect. A set of highly invasive breast‐carcinoma cells (MDA‐231, BT‐549, HS‐578t) neither adhered to nor rolled on resting or TNF‐stimulated endothelial cell monolayers. However, after 5 min of static incubation, a fraction of these cells attached strongly to resting and TNF‐stimulated endothelial cells and this static adhesion could not be blocked by an E‐selectin‐specific monoclonal antibody. Our results suggest that E‐selectin is a major homing receptor in the metastasis of some breast and colon cancers. © 1995 Wiley‐Liss, Inc.