492 Altered focal adhesion pattern of G0-positive melanoma cells

Cancer cell drug resistance develops via several mechanisms, including apoptosis evading, efflux, reprogramming, DNA repair. Recently numerous data pointed out an ability of cancer cells reversibly exit from cycle to enter in G0 phase that may favor survival. Therefore, the goal study was determine transcriptional phenotype associated with quiescent/senescent state acquisition. Melanoma were treated by Dacarbazine induce their transition a followed Ki-67 and flow cytometry-based analysis. Beta-galactosidase expression identified hydrolysis 5-bromo-4-chloro-3-indolyl β-D-galactopyranoside resulting blue staining beta-galactosidase positive cells. Microarray performed access profiling alterations. Cell adhesion capacities G0-positive determined centrifugal force. Indeed, 1.2 mmol induced 4-fold increase percentage BRO SK-MEL-2 also visualized immunostaining. Opposite, beta-galactosidase-positive increased 0.3 0.7% did not altered According transcriptomic top signal pathways enriched among dysregulated genes «Cell cycle», «p53 gene network», «Focal adhesion». Next, assay melanoma following treatment Dacarbazine. Both exhibited elevated adhesive In conclusion, human under results significant alterations profile. Besides, demonstrated enhanced be related pre-metastatic niche formation dissemination.