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Inhibition of MCF‐7 breast cancer cell proliferation by MCF‐10A breast epithelial cells in coculture
Author(s) -
Spink Barbara C.,
Cole Richard W.,
Katz Barbara H.,
Gierthy John F.,
Bradley Laurie M.,
Spink David C.
Publication year - 2006
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2005.11.006
Subject(s) - mcf 7 , paracrine signalling , matrigel , green fluorescent protein , cell growth , microbiology and biotechnology , cancer cell , biology , autocrine signalling , cell , cell culture , chemistry , cancer , biochemistry , receptor , genetics , human breast , gene
A coculture system was developed to investigate the interactions between MCF‐10A breast epithelial cells and MCF‐7 breast cancer cells stably expressing the green fluorescent protein (MCF‐7‐GFP). Studies with this MCF‐10A/MCF‐7‐GFP coculture system on microtiter plates and on reconstituted basement membrane (Matrigel), revealed paracrine inhibition of MCF‐7‐GFP cell proliferation. Epidermal growth factor, which in monocultures modestly enhanced MCF‐7‐GFP and markedly increased MCF‐10A cell proliferation, greatly inhibited MCF‐7‐GFP cell proliferation in MCF‐10A/MCF‐7‐GFP cocultures. 17β‐Estradiol, which stimulated MCF‐7‐GFP but not MCF‐10A cell proliferation in monoculture, inhibited MCF‐7‐GFP cell proliferation in MCF‐10A/MCF‐7‐GFP cocultures, an effect that was blocked by the antiestrogen, ICI 182,780. On Matrigel, complex MCF‐10A/MCF‐7‐GFP cellular interactions were observed in real time that resulted in the formation of acinus‐like structures. These results indicate a role of normal epithelial cells in inhibiting tumor‐cell proliferation and demonstrate the utility of this coculture system as a model of early paracrine control of breast cancer.