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Effect of stromal and epithelial cells derived from normal and tumorous breast tissue on the proliferation of human breast cancer cell lines in co‐culture
Author(s) -
Bourhis Xuefen DongLe,
Berthois Yolande,
Millot Guy,
Degeorges Armelle,
Sylvi Monique,
Martin PierreMarie,
Calvo Fabien
Publication year - 1997
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/(sici)1097-0215(19970328)71:1<42::aid-ijc9>3.0.co;2-3
Subject(s) - stromal cell , paracrine signalling , cell culture , cancer research , biology , cell growth , epithelium , pathology , cell , cancer cell , cell type , breast cancer , cancer , medicine , receptor , biochemistry , genetics
Stromal and epithelial components surrounding neoplastic cells are believed to be important in tumor regulation. We have studied the effects of stromal and epithelial cells on the proliferation of a variety of breast‐cancer epithelial cell lines. Co‐culture experiments were performed in which the 2 cell types were separated by a microporous membrane. Under these conditions, fibroblasts from normal breast tissues inhibited the proliferation of MCF‐7 cells, but not that of immortalized normal S2T2 cells. In contrast, fibroblasts from cancerous breast tissues did not influence the proliferation of the 2 cell lines tested. Conditioned media (CM) of breast fibroblasts derived from normal tissues were not able to affect MCF‐7 cell growth, suggesting complex paracrine interactions between both cell types. Normal breast epithelial cells (NBEC) have also been tested for their ability to regulate the proliferation of breast‐cancer epithelial cell lines. Co‐culture experiments demonstrated that NBEC inhibited a variety of breast‐cancer cell lines. CM from NBEC induced similar results and the inhibitory effect appeared to be specific for epithelial cells from tumorous breast. Moreover, CM from NBEC and normal fibroblasts were shown to contain more TGF β1 and amphiregulin than those of MCF‐7 cells. We conclude that both the tissue origin and the target tumor cell's phenotype will determine the extent of proliferative response. More important, the tumor‐cell growth inhibition induced by fibroblasts and epithelial cells of normal breast tissue may constitute a tumor‐growth‐regulatory mechanism. Int. J. Cancer, 71:42–48, 1997. © 1997 Wiley‐Liss, Inc.