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EXTRACELLULAR MATRIX REMODELLING IN A MURINE MAMMARY ADENOCARCINOMA TRANSFECTED WITH THE INTERFERON‐ALPHA1 GENE
Author(s) -
SCARPA SUSANNA,
GIUFFRIDA ANNA,
PALUMBO CAMILLA,
VASATURO FORTUNATA,
SIGNORELLI PAOLA,
FORNI GUIDO,
MODESTI MAURO,
FERRANTINI MARIA,
BELARDELLI FILIPPO,
MUSIANI PIERO,
MODESTI ANDREA
Publication year - 1997
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199701)181:1<116::aid-path116>3.0.co;2-x
Subject(s) - stromal cell , transfection , fibroblast , fibronectin , extracellular matrix , microbiology and biotechnology , cd8 , interferon , cancer research , chemistry , biology , cell culture , in vitro , immunology , immune system , biochemistry , genetics
The rejection of interferon alpha1 gene‐transfected mammary adenocarcinoma cells (TSA‐IFNα) injected into syngeneic BALB/c mice was accompanied by an unusual stromal reaction and marked CD8‐positive T‐lymphocyte involvement. To investigate the biological background of this reaction, the possibility was evaluated that an interaction between TSA‐IFNα and stromal cells might remodel the extracellular matrix (EM). When fibroblasts were co‐cultured with TSA‐IFNα or treated with exogenous IFNα, there was no change in their replication rate or collagen synthesis. By contrast, their fibronectin (FN) production and release were increased, resulting in enhanced fibroblast chemotaxis. These findings were mirrored by increased FN staining in the peritumoural and tumoural areas in vivo . IFNα thus determines increased FN production and hence massive local recruitment and activation of fibroblasts, with a modification of the EM. The several activities of IFNα should thus be considered prior to its employment in clinical trials. © 1997 by John Wiley & Sons, Ltd.