Abstract

Cancer cell drug resistance develops via several mechanisms, including apoptosis evading, drug efflux, cell reprogramming, DNA repair. Recently numerous data pointed out an ability of cancer cells reversibly exit from cell cycle to enter in G0 phase that may favor cancer cell survival. Therefore, the goal of the study was to determine transcriptional phenotype associated with quiescent/senescent state acquisition. Melanoma cells were treated by Dacarbazine to induce their transition in G0 phase of a cell cycle followed by Ki-67 and flow cytometry-based cell cycle analysis.

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