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Expression of different tenascin isoforms in normal, hyperplastic and neoplastic human breast tissues
Author(s) -
Borsi Laura,
Carnemolla Barbara,
Nicolò Guido,
Spina Bruno,
Tanara Giorgio,
Zardi Luciano
Publication year - 1992
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.2910520504
Subject(s) - gene isoform , pathology , tenascin , human breast , biology , medicine , breast cancer , cancer research , microbiology and biotechnology , cancer , extracellular matrix , genetics , gene , fibronectin
Functionally different tenascin (TN) isoforms, containing varying numbers of a 91 amino‐acid motif resembling the fibronectin type‐III homology repeat, may be generated by alternative splicing of the TN primary transcript. In fact, only the TN isoform containing the alternatively spliced region can induce loss of focal adhesion in cultured cells and seems to be able to facilitate cell migration. We examined the patterns of alternative splicing of the TN primary transcript in normal, hyperplastic and neoplastic breast tissues, and found that, in all the invasive breast carcinomas analyzed, the relative amount of TN mRNA in which the alternatively spliced region was included was about 10 times higher than in RNA from normal breast tissues. A similar result was observed in phyllodes tumors and in those fibroadenomas which showed very high stromal cellularity. Western‐blot analysis using different monoclonal antibodies showed the same pattern as that seen in Northern blotting. The data reported here suggest that, in the breast, expression of the high‐molecular‐mass TN isoform is a marker of stromal element proliferation and that, in invasive breast carcinomas, this TN isoform could play a role in generating a permissive environment for proliferation, invasion and metastasis of neoplastic epithelial cells. © 1992 Wiley‐Liss, Inc.