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CD44 signaling through focal adhesion kinase and its anti‐apoptotic effect
Author(s) -
Fujita Yoshihisa,
Kitagawa Motoo,
Nakamura Sukeyuki,
Azuma Kazuhiko,
Ishii Genichiro,
Higashi Morihiro,
Kishi Hirohisa,
Hiwasa Takaki,
Koda Keiji,
Nakajima Nobuyuki,
Harigaya Kenichi
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03262-3
Subject(s) - focal adhesion , cd44 , apoptosis , microbiology and biotechnology , chemistry , signal transduction , kinase , adhesion , cancer research , biochemistry , biology , cell , organic chemistry
Adhesion molecules can initiate intracellular signaling. Engagement of CD44 either by its natural ligand hyaluronan or a specific antibody on a cell line induced tyrosine phosphorylation and activation of focal adhesion kinase (FAK), which then associated with phosphatidylinositol 3‐kinase (PI3K) and activated mitogen‐activated protein kinase at its downstream. However, the introduction of dominant negative Rho into the cells inhibited the CD44‐stimulated FAK phosphorylation. Cells expressing CD44 were significantly resistant to etoposide‐induced apoptosis. This anti‐apoptotic effect was cancelled by the inhibition of either Rho, FAK or PI3K. These results may indicate a signaling pathway from CD44 to mediate the resistance against drug‐induced apoptosis in cancer cells.