Overexpression of melanoma inhibitory activity (MIA) enhances extravasation and metastasis of A-mel 3 melanoma cells in vivo

Guba, Markus and Bosserhoff, Anja-Katrin and Steinbauer, M. and Abels, C. and Anthuber, M. and Buettner, R. and Jauch, K. W. (2000) Overexpression of melanoma inhibitory activity (MIA) enhances extravasation and metastasis of A-mel 3 melanoma cells in vivo. BRITISH JOURNAL OF CANCER, 83 (9). pp. 1216-1222. ISSN 0007-0920, 1532-1827

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Abstract

The secreted MIA protein is strongly expressed by advanced primary and metastatic melanomas but not in normal melanocytes. Previous studies have shown that MIA serum levels correlate with clinical tumour progression in melanoma patients. To provide direct evidence that MIA plays a role in metastasis of malignant melanomas, A-mel 3 hamster melanoma cells were transfected with sense- and antisense rhMIA cDNA and analysed subsequently for changes in their tumorigenic and metastatic potential. Enforced expression of MIA in A-mel 3 cells significantly increased their metastatic potential without affecting primary tumour growth, cell proliferation or apoptosis rate in hamsters, compared with control or antisense transfected cells. Additionally, MIA overexpressing transfectants showed a higher rate of both tumour cell invasion and extravasation. Cells transfected with MIA antisense generally exerted an opposite response. The above changes in function attributed to the expression of MIA may underlie the contribution of MIA to the malignant phenotype, (C) 2000 Cancer Research Campaign.

Item Type: Article
Uncontrolled Keywords: MALIGNANT-MELANOMA; EXPRESSION; CANCER; GENE; TRANSFORMATION; TUMORIGENICITY; PROTEINS; ADHESION; HAMSTER; LIVER; MIA; intravital microscopy; tumour cell invasion; melanoma
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Chirurgie
Medicine > Lehrstuhl für Dermatologie und Venerologie
Depositing User: Dr. Gernot Deinzer
Date Deposited: 16 Mar 2022 15:44
Last Modified: 16 Mar 2022 15:44
URI: https://pred.uni-regensburg.de/id/eprint/42071

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