IDH-mutant ATRX loss/intact GL261 RNA-seq and IDH-mutant human gliomas RNA-seq

ATRX (alpha-thalassemia/mental retardation syndrome X-linked) is a critical chromatin remodeling factor widely implicated in glioma pathobiology, especially in IDH-mutant low-grade gliomas where ATRX loss frequently occurs. ATRX deficiency synergizes with mutant IDH1 to promote genome instability, modify gene expression networks, and alter tumor phenotypes. Importantly, ATRX loss has been associated with regulation of cellular senescence, the senescence-associated secretory phenotype (SASP), and immune cell recruitment within the glioma microenvironment. Mouse glioma GL261 cells were cultured in DMEM (high glucose) supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin. To generate IDH-mutant GL261 cells with or without ATRX deficiency, mut-IDH1R132H and shRNA targeting murine Atrx (CCCACGGATGAGAATGTAAAT; both from Genechem, China) were stably introduced to establish IDH-mutant GL261 cells with intact or loss of ATRX function.