## Abstract ADAMβ9 belongs to a family of transmembrane disintegrinβcontaining metalloproteinases (ADAMs) involved in protein ectodomain shedding and cellβcell and cellβmatrix interactions. However, the specific biological functions of ADAMβ9 are still unclear. The aim of this study was to analyze
Expression and function of CD9 in melanoma cells
β Scribed by Jun Fan; Guo-Zhang Zhu; Richard M. Niles
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 267 KB
- Volume
- 49
- Category
- Article
- ISSN
- 0899-1987
- DOI
- 10.1002/mc.20580
No coin nor oath required. For personal study only.
β¦ Synopsis
CD9, a member of the tetraspanin family, functions as an organizer in "tetraspanin webs," through interacting with other cell adhesion molecules. It plays a role in differentiation, fertilization, and cell migration. We investigated the expression and function of CD9 in melanoma. CD9 protein expression in B16 mouse melanoma and six human melanoma cell lines was decreased compared to normal melanocytes. B16F1 clones stably overexpressing CD9 had reduced ability to form colonies in soft agar; however, paradoxically these overexpressing clones had increased ability to invade Matrigel. Similarly, transient overexpression of CD9 in the human metastatic melanoma cell line WM9 dramatically decreased anchorage-independent growth, while transient overexpression of CD9 in the radial growth phase cell line SbCl2 resulted in the gain of Matrigel invasion activity. DNA sequencing of CD9 cDNA from all six human melanoma cell lines did not show deletions, insertions, or mutations. Treatment of all six human melanoma cell lines with the histone deacetylase inhibitor trichostatin A increased CD9 levels. The DNA methylation inhibitor 5-aza-cytidine also increased CD9 protein levels with greater increases seen in cell lines derived from more malignant melanomas.
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We have previously shown that one of the co-factors required for generation of T-cell responses, 87. I, is variably expressed on melanoma cells. In the present studies we have examined the expression of another important co-factor in T-cell responses, viz., CD40, and investigated regulation of its e