Project description:Glioblastoma is the most common primary malignant brain tumor with an unfavorable prognosis and a reprogrammed metabolism. In order to define the role of lactic acid in the context of glioblastoma epigenetic remodeling, pediatric GBM cells, KNS42, were growth for 24h in different media conditions (starvation media -0.5mM Glucose; 0.5mM Glutamate or physiological media -5mM Glucose; 0mM Glutamate) with or without L-lactic acid for 24h. Thereafter, cells were harvested and samples were subjected to ChIP isolation using H3K27ac and H3K9ac antibodies. DNA was subsequently processed for CHIP sequencing to assess epigenetic changes mediated by lactic acid.
Project description:We over-expressed an epigenetic regulator in a glioblastoma (GBM) primary culture from an adult patient. These GBM cells have cancer stem cell phenotypes, as they have self-renewal properties and tumor initiation potential when transplanted in immunocompromised mice. ATAC-seq was performed on cells over-expressing the epigenetic regulator and control cells expressing EGFP. ATAC-Seq on glioblastoma cells that over-express EGFP or an epigenetic regulator.
Project description:Chromatin accessibility was profiled by ATAC-seq in normal and glioblastoma-derived neural stem (GNS) cells, in self-renewing conditions and in response to differentiation stimulus with bone morphogenic protein (BMP).
Project description:Recently, L-lactic acid was identified as a unique metabolite in periapical granulomas. However, the biological roles of this metabolite in this lesion were unknown. Therefore, we aimed to investigate the inflammatory effect of L-lactic acid on peripheral blood mononuclear cells (PBMCs).