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Tyrosine kinase inhibitor TKI ‐258 inhibits cell motility in oral squamous cell carcinoma in vitro
Author(s) -
Carneiro Anna Cecília Dias Maciel,
Silveira Isadora Caixeta da,
Rezende Arthur Silva,
Silva Bruna Raphaela Oliveira,
Crema Virgínia Oliveira
Publication year - 2017
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12511
Subject(s) - matrigel , biology , cell , tyrosine kinase , motility , platelet derived growth factor receptor , cell migration , microbiology and biotechnology , cancer research , receptor , signal transduction , biochemistry , growth factor
Background Oral squamous cell carcinoma is extremely invasive, and this behavior is regulated by binding of extracellular molecules to the cell membrane receptors. The TKI ‐258 inhibits phosphorylation of FGFR s VEGFR s and PDGFR s. Our aim was to analyze the effect of TKI ‐258 treatment in cell movement using SCC ‐4 cell line from human oral squamous cell carcinoma. Methods F‐actin was stained with rhodamine phalloidin, and confocal analysis was performed. The migration and invasion (membrane covered with Matrigel ™ ) three‐dimensional assays were performed, and control and cells treated with TKI ‐258 that migrated through the membrane were counted after 24 h. Results Control cells presented abundant cytoplasm with F‐actin wide distributed and evident cell cortex; however, treated (1, 5 and 10 μM TKI ‐258) cells showed round morphology, scanty cytoplasm, F‐actin disorganized and preserved cell cortex. TKI ‐258 (1, 5, and 10 μM) treatment inhibits migrating cells ( ANOVA , F = 97.749, d.f. = 3, 10; P < 0.0001), and it was concentration dependent. Invading cell treated with 5 μM TKI ‐258 was significantly lower ( t = 6.708, d.f. = 5, P < 0.001). Conclusions These results suggest that the tyrosine kinase inhibitor TKI ‐258 has an inhibitory effect on cell motility, affecting F‐actin, cell migration, and cell invasion, and probably, these processes are regulated by signaling pathways FGFR s and/or PDGFR s and/or VEGFR s.