Opposite regulation of tenascin-C and tenascin-X in MeLiM swine heritable cutaneous malignant melanoma

Citation
C. Geffrotin et al., Opposite regulation of tenascin-C and tenascin-X in MeLiM swine heritable cutaneous malignant melanoma, BBA-GEN SUB, 1524(2-3), 2000, pp. 196-202
Citations number
37
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
ISSN journal
03044165 → ACNP
Volume
1524
Issue
2-3
Year of publication
2000
Pages
196 - 202
Database
ISI
SICI code
0304-4165(200012)1524:2-3<196:OROTAT>2.0.ZU;2-2
Abstract
Interactions between tumour cells and surrounding extracellular matrix (ECM ) influence the growth of tumour cells and their ability to metastasise. It is thus interesting to compare ECM composition in tumours and healthy tiss ues. Using the recently described MeLiM miniature pig model of heritable cu taneous malignant melanoma, we studied the expression of two ECM glycoprote ins, the tenascin-C (TNC) and tenascin-X (TN-X), in normal skin and melanom a. Using semiquantitative RT-PCR, we observed a 3.6-fold mean increase of T N-C RNAs in melanoma compared to normal skin. Both stromal and tumour cells synthesise TN-C. On the contrary, TN-X RNAs decreased 30-fold on average i n melanoma. This opposite regulation of TN-C and TN-X RNAs was confirmed at the protein level by indirect immunofluorescence. Whereas pig normal skin displayed a discrete TN-C signal at the dermo-epidermal junction, around bl ood vessels and hair bulbs, the swine tumour showed enhanced expression of TN-C in these areas and around stromal and tumour cells. In contrast, norma l skin showed a strong TN-X staining at the dermo-epidermal junction and in the dermis, whereas this signal almost completely disappeared in the tumou r. The results presented here describe a dramatic alteration of the ECM com position in swine malignant melanoma which might have a large influence on tumourigenesis or invasion and metastasis of melanoma cells. (C) 2000 Elsev ier Science B.V. All rights reserved.