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Inhibition of melanoma cell directional migration in vitro via different cellular targets
Author(s) -
FinkPuches Regina,
Helige Christine,
Kerl Helmut,
Smolle Josef,
Tritthart Helmut A.
Publication year - 1993
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1993.tb00194.x
Subject(s) - calmodulin , motility , verapamil , melanoma , signal transduction , cell migration , antagonist , in vitro , chemistry , microbiology and biotechnology , cancer research , pharmacology , biology , receptor , calcium , biochemistry , enzyme , organic chemistry
In malignant melanoma active movement of cancer cells is considered to be essential for tissue invasion. Various mechanisms, such as the Ca 2+ ‐calmodulin‐proteinkinase C cascade or G‐protein‐dependent processes are considered to play a role in tumor cell functions. The assay of directional migration, combined with computer‐assisted image analysis, was used to evaluate the antimigratory efficacy of drugs interfering with different steps of signal (ransduction pathways. Treatment with different compounds showed a more or less concentration‐dependent reduction of migration rates: The Ca 2+ ‐channel blockers verapamil and devapamil showed a slight reduction of molility. The effect was more pronounced when the calmodulin antagonist flunarizine was used or the proteinkinase C inhibitors dequalinium, tamoxifen and H‐7 were applied. A marked inhibition of molility was found with the G‐protein antagonist L 651582. Thus, our results indicate that different signal transduclion pathways are involved in the regulation of directional migration of K1735‐M2 melanoma cells.