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Synthesis and protein distribution of the unspliced large tenascin‐C isoform in oral squamous cell carcinoma
Author(s) -
Hindermann Winfried,
Berndt Alexander,
Borsi Laura,
Luo Xinmei,
Hyckel Peter,
Katenkamp Detlef,
Kosmehl Hartwig
Publication year - 1999
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(199912)189:4<475::aid-path462>3.0.co;2-v
Subject(s) - stromal cell , tenascin c , biology , in situ hybridization , immunohistochemistry , microbiology and biotechnology , stroma , carcinoma , extracellular matrix , messenger rna , pathology , cancer research , medicine , immunology , gene , biochemistry
The inclusion or omission of the alternatively spliced region in the tenascin‐C (Tn‐C) mRNA gives rise to the large (Tn‐C L ) or small (Tn‐C S ) variant, respectively. Tn‐C L is thought to be a typical component of provisional extracellular matrices (ECMs) and is expressed during tumour stroma remodelling. Tn‐C L synthesis has been studied using RNA/RNA in situ hybridization, and Tn‐C L protein distribution, using immunohistochemistry (clone BC‐2), in 18 oral squamous cell carcinomas (OSCCs) of different grades of malignancy. While the Tn‐C L protein was demonstrated within the whole stromal compartment regardless of grade of malignancy, the majority of the Tn‐C L mRNA signal‐bearing cells were carcinoma cells. Only a few stromal myofibroblasts were able to synthesize Tn‐C L , as revealed by α‐smooth muscle actin double staining. In well‐differentiated carcinomas (G1), the Tn‐C L synthesizing carcinoma cells were localized as a single positive cell layer in the tumour stroma interface, particularly in invasive areas. A higher grade of malignancy (G2/G3) is associated with a significantly increased number of Tn‐C L synthesizing carcinoma cells randomly distributed within the invading tumour areas. Double‐staining experiments (Tn‐C L mRNA ISH/BC‐2 immunohistochemistry) indicate that these cells are capable of organizing and depositing a three‐dimensional Tn‐C L matrix. Even though an instructive and/or inductive role of the carcinoma cells in tumour stroma formation cannot be excluded, these results demonstrate that carcinoma cells can directly produce the ECM components of tumour stroma. Copyright © 1999 John Wiley & Sons, Ltd.

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