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J Biol Chem, Vol. 273, Issue 26, 16501-16508, June 26, 1998
From the MCAM/MUC18 is a cell-surface glycoprotein of 113 kDa, originally identified as a melanoma antigen, whose expression is
associated with tumor progression and the development of metastatic
potential. We have previously shown that enforced expression of
MCAM/MUC18 in primary cutaneous melanoma led to increased tumor growth
and metastatic potential in nude mice. The mechanism for up-regulation of MCAM/MUC18 during melanoma progression is unknown. Here we show that
up-regulation of MCAM/MUC18 expression in highly metastatic cells
correlates with loss of expression of the transcription factor AP-2.
The MCAM/MUC18 promoter contains four binding sites for AP-2, and
electrophoretic mobility shift assay gels demonstrated that the AP-2
protein bound directly to the MCAM/MUC18 promoter. Transfection of AP-2
into highly metastatic A375SM melanoma cells (AP-2-negative and
MCAM/MUC18-positive) inhibited MCAM/MUC18 promoter-driven chloramphenicol acetyltransferase reporter gene in a
dose-dependent manner. MCAM/MUC18 mRNA and protein
expression were down-regulated in AP-2-transfected but not in control
cells. In addition, re-expression of AP-2 in A375SM cells inhibited
their tumorigenicity and metastatic potential in nude mice. These
results indicate that the expression of MCAM/MUC18 is
regulated by AP-2 and that enforced AP-2 expression suppresses
tumorigenicity and metastatic potential of human melanoma cells,
possibly by down-regulating MCAM/MUC18 gene expression. Since AP-2 also regulates other genes that are
involved in the progression of human melanoma such as
c-KIT, E-cadherin, MMP-2, and p21WAF-1,
we propose that loss of AP-2 is a crucial event in the development of
malignant melanoma.
Loss of AP-2 Results in Up-regulation of
MCAM/MUC18 and an Increase in Tumor Growth and
Metastasis of Human Melanoma Cells
,,,,,
Department of Cell Biology and the
§ Department of Tumor Biology, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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