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Human Molecular Genetics Advance Access published online on August 18, 2008
Human Molecular Genetics, doi:10.1093/hmg/ddn252
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Expression of p21waf1/Cip1 in stromal fibroblasts of primary breast tumors

George Trimis1, Ioulia Chatzistamou2, Katerina Politi3, Hippokratis Kiaris1 and Athanasios G. Papavassiliou1

1 Department of Biological Chemistry, University of Athens Medical School, 75 M. Asias str., 115 27 Athens, Greece 2 Department of Histology and Embryology, University of Athens Medical School, 75 M. Asias str., 115 27 Athens, Greece 3 Department of Cytopathology, Aretaieion Hospital, University of Athens Medical School, 115 27 Athens, Greece

Correspondence: Dr Hippokratis Kiaris, Department of Biological Chemistry, University of Athens Medical School, 75 M. Asias str., 115 27 Athens, Greece hkiaris{at}med.uoa.gr

Received August 11, 2008; Revised August 15, 2008; Accepted August 15, 2008

During carcinogenesis stromal fibroblasts undergo certain changes in concert with their neoplastic neighbors, an interaction that progressively leads to a cancer-associated state. Despite however the increasing appreciation of the importance of stromal/tumor interactions in the progression of cancer, little is known about the factors responsible for regulating the crosstalk between stromal fibroblasts and neoplastic cells. Here we show that the stage of the disease in primary human breast lesions affects p21 expression in the fibroblasts: In stromal fibroblasts of benign fibroadenomas p21 exhibits a periductal pattern of staining that is abolished in malignant adenocarcinomas at which p21 immunopositivity exhibits a mosaic pattern that eventually is abolished in more aggressive types of the disease. In order to address the role of fibroblasts’ p21 in tumorigenesis we have reconstituted MCF7 human breast cancers in mice, with fibroblasts differing in the p21 status. These experiments showed that p21 deficiency in stromal fibroblasts accelerates tumor growth through cell non-autonomous mechanism(s). In addition, even a transient siRNA-mediated p21 suppression in fibroblasts, sufficiently stimulates MCF7 and MDA-MB-231 growth in vivo. We propose that p21 regulation is intimately linked with the ability of stromal cells to affect tumor growth.


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