Exp Mol Med.  2002 Jul;34(3):177-183.

Functional involvement of src and focal adhesion kinase in a CD99 splice variant-induced motility of human breast cancer cells.

Affiliations
  • 1Vascular System Research Center, College of Natural Sciences, Kangwon National University, Chunchon, Korea.
  • 2Division of Life Sciences, College of Natural Sciences, Kangwon National University, Chunchon, Korea.

Abstract

Earlier report showed that expression of a splice variant of CD99 transmembrane protein increases invasive ability of human breast cancer cells. Cell motility was also significantly enhanced by the CD99 splice variant expression. In an effort to identify the cellular components that mediate a signal transduction pathway triggered by the CD99 splice variant, known signal path inhibitors were examined for their effects on the motility of the CD99 splice variant-transfected MDA-MB-231 breast cancer cells. Phenylarsine oxide, an inhibitor of phosphatase specific for focal adhesion kinase, and PP1, an inhibitor of src kinase family, significantly suppressed motility of the cells. Among different types of src transfectant clones generated, kinase-negative mutant src transfectant cells were 80% less motile than the mock cells transfected with an empty-vector, while v-src and c-src transfectants exhibited cell motility levels at or slightly above the mock transfectant. These results suggest that src and focal adhesion kinase mediate the intracellular signaling pathway of a CD99 splice variant for the induction of motility of human breast cancer cells.

Keyword

breast cancer; CD99; focal adhesion kinase; motility; splice variant; src

MeSH Terms

Antigens, CD/*genetics
Arsenicals/pharmacology
Breast Neoplasms/*enzymology/genetics/*pathology
Cell Adhesion Molecules/*genetics
Cell Movement/drug effects
Gene Expression
Protein-Tyrosine Kinase/antagonists & inhibitors/*metabolism
Pyrazoles/pharmacology
Pyrimidines/pharmacology
Signal Transduction/drug effects
Transfection
Tumor Cells, Cultured
src-Family Kinases/antagonists & inhibitors/*metabolism
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