Functional involvement of src and focal adhesion kinase in a CD99 splice variant-induced motility of human breast cancer cells..
- Author:
Hyuk Joon LEE
1
;
Eun Sook KIM
;
Bok Eun JEE
;
Jang Hee HAHN
;
Kyu Hyoung HAN
;
Kyeong Cheon JUNG
;
Seong Hoe PARK
;
Han Soo LEE
Author Information
1. Vascular System Research Center, College of Natural Sciences, Kangwon National University, Chunchon, Korea.
- Publication Type:Original Article
- Keywords:
breast cancer;
CD99;
focal adhesion kinase;
motility;
splice variant;
src
- MeSH:
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
- From:Experimental & Molecular Medicine
2002;34(3):177-183
- CountryRepublic of Korea
- Language:English
-
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.
