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The role of the sodium hydrogen exchanger in stress fiber formation in human lung cancer stimulated with urokinase plasminogen activator, lysophosphatic acid, and phenylephrine
Author(s) -
Canine Jenny,
Wallert Mark A,
Provost Joseph J
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1029.5
Subject(s) - stress fiber , chemistry , cell migration , microbiology and biotechnology , plasminogen activator , cancer research , biophysics , cytoskeleton , cell , endocrinology , biochemistry , biology
One of cancers hallmarks is the ability of cells to spread from the tumor of origin to other areas of the body, a process called metastastis. The Sodium‐Hydrogen Exchanger (NHE) plays a role in pH regulation and cytoskeletal attachment to the plasma membrane. In studies using CCL39 lung fibroblasts, phenylephrine (PE) induced stress fibers, and caused cells to become tumor like. In wound assay studies, PE stimulated stress fiber formation in cells immediately adjacent to the wound area and in migrating cells. These data indicate that stress fiber formation has a direct involvement in cell migration. In this study, we relate data from CCL39 cells to stress fiber formation in human lung cancer. We studied stress fiber formation in H358, H460, and H1299 cells. Our data shows that in H358 cells both 50μM PE and 10nM urokinase‐type plasminogen activator (uPA) significantly increase stress fiber formation. In H460 cells, 3μM lysophosphatidic acid (LPA) and UPA significantly increase stress fiber formation, and in H1299 all three hormones significantly increase stress fiber formation. Our data also shows that using ethylisopropylamiloride to inhibit NHE decreases the level of stress fiber formation in H460 and H1229 cells. These studies indicate that NHE plays a vital role in stress fiber formation and cellular migration, metastasis, in human lung cancer cells.