Melanoma-Associated Antigen Family Protein-D1 Regulation of Tumor Cell Migration, Adhesion to Endothelium, and Actin Structures Reorganization in Response to Hypoxic Stress

Melanoma-associated antigen family protein-D1 (MAGE-D1) is a recently identified p75 neurotrophin receptor intracellular binding protein and functions as an adaptor that mediates multiple signaling pathways, including Dlx/Msx-mediated transcription. Here, a new regulatory function for MAGE-D1 in tum...

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Bibliographic Details
Published in:Cell communication & adhesion 2007, Vol.14 (1), p.21-31
Main Authors: Shen, Wei-Gan, Xue, Qing-Yu, Wu, Yi-Ding, Hu, Ben-Shun, Zhu, Jun, Zhang, Yu, Su, Qing
Format: Article
Language:English
Subjects:
actin
Actins - chemistry
Actins - metabolism
Adenoviridae - genetics
adhesion
Antigens, Neoplasm - metabolism
Blotting, Western
Cell Adhesion
Cell Hypoxia
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cytoskeleton - metabolism
Endothelium - pathology
Gene Expression Regulation, Neoplastic
Genes, Reporter
HeLa Cells
Humans
hypoxia
Hypoxia-Inducible Factor 1 - genetics
invasion
melanoma-associated antigen family protein-D1 (MAGE-D1)
migration
Neoplasm Invasiveness
Neoplasm Proteins - metabolism
Neoplasms - metabolism
Neoplasms - pathology
Pseudopodia - metabolism
Wound Healing
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Summary:Melanoma-associated antigen family protein-D1 (MAGE-D1) is a recently identified p75 neurotrophin receptor intracellular binding protein and functions as an adaptor that mediates multiple signaling pathways, including Dlx/Msx-mediated transcription. Here, a new regulatory function for MAGE-D1 in tumor cell motility and adhesion to endothelium is described. MAGE-D1 over-expression suppressed HeLa cell and BEL7402 cell migration, invasion, and adhesion to the monolayer of ECV304 cells. We also report that MAGE-D1 over-expression disrupted actin cytoskeleton rearrangement induced by hypoxia and down-regulated hypoxia inducible factor 1-dependent luciferase gene expression. These findings provide new insight into the ability of MAGE-D1 to suppress the motility and adhesion response of tumor cells by interfering with actin cytoskeleton reorganization and hypoxia inducible factor 1-dependent gene expression.
ISSN:1541-9061
1543-5180
DOI:10.1080/15419060701224948