MiR-155-5p-mediated increase in p53 content induced by dacarbazine in melanoma cells

BACKGROUND: Cellular senescence is a stress response, triggered by various stimuli such as chemotherapy treatment and causes G0/G1 cell cycle arrest followed the production of associated secretory phenotype. p53 considered to be modulator these events although precise mechanisms it remains not clear.
 AIMS: To determine non-apoptotic functions protein formation phenotype melanoma cells under cytostatic agent dacarbazine.
 MATERIALS AND METHODS: The study was conducted on BRO SK-MEL-2 skin lines. Melanoma were treated dacarbazine. Then immunocytochemical performed proportion G0-positive expression tumor suppressor p53. A bioinformatic analysis accomplished identify for regulators with determining miR-155-5p levels in exosomes released dacarbazine-treated cells.
 RESULTS: drug dacarbazine increases residing G0 phase cycle. Onco-microRNA expressed two studied lines melanoma. Changes level correlate changes microRNA expression. absence may due levels. In line, no oncosuppressor observed an increased percentage cells, which activation other phase.
 CONCLUSIONS: Heterogeneous effect revealed. For induces release inhibiting exosomal miR-155-5p, activates oncosuppressor, line.