KDM1A represses the apoptosis in osteosarcoma cells via demethylating Bcl-2/c-Myc

Introduction Background: Considering the poorly understood mechanism of lysine demethylase 1A (KDM1A) in osteosarcoma (OS), we here commence our investigation to fill blank. Material and methods Methods: Following transfection as appropriate, 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) flow cytometry assays were used determine viability apoptosis OS cells MG-63, which generation reactive oxygen species (ROS) binding between KDM1A Bcl-2/ cellular Myc (c-Myc) separately confirmed via DCF-DA method chromatin immunoprecipitation-PCR. Reverse-transcription quantitative PCR western blot finally introduced quantify levels KDM1A/Bcl-2/c-Myc endoplasmic reticulum (ER) stress-related factors. Results Results: Overexpressed enhanced (48 hours) yet repressed ROS generation, with downregulation on ER factors (C/EBP homologous protein [CHOP]; proline-rich extensin-like receptor kinase (PERK) activating transcription factor 4 [ATF4]) elevation Bcl-2/c-Myc, while its depletion exerted contrary effects. More importantly, could act reflected by results that decreased enrichment Bcl-2/c-Myc promoter using antibody against increased targeting H3K9me2. silencing, conversely, promoted apoptosis, elevated abolished effects cells. Conclusions Conclusion: exerts a repressive effect MG-63 inhibiting stress demethylation Bcl-2 c-Myc.