ChIP-seq of BORIS in U87MG cells
Glioblastoma multiforme (GBM) remains one of the most aggressive and lethal brain tumors, characterized by extensive molecular heterogeneity and limited therapeutic options. BORIS (CTCFL), a paralog of the chromatin insulator CTCF, functions as an epigenetic and transcriptional regulator implicated in multiple cancers; however, its role in GBM is poorly understood. Here, we show that BORIS contributes to the regulation of gene networks underlying tumor-intrinsic and microenvironmental programs in GBM. Integrative analyses of TCGA-GBM and GTEx brain cortex transcriptomic data revealed that BORIS expression is significantly elevated in GBM. To explore its regulatory function, we performed ChIP-seq profiling in U87MG cells, showing that BORIS binding is predominantly enriched at promoter regions of genes involved in development, morphogenesis, and transcriptional control. Integration of ChIP-seq and differential expression data identified CD36 (a fatty acid transporter) and FBN2 (an extracellular matrix component linked to TGFß signaling) as potential direct BORIS targets. ChIP-qPCR confirmed BORIS occupancy at their promoters, while RT-qPCR demonstrated transcriptional upregulation of both genes upon BORIS overexpression. These findings support a model in which BORIS acts as a transcriptional hub that potentially links oncogenic signaling, stemness, and extracellular matrix remodeling. By activating targets such as CD36 and FBN2, BORIS may promote metabolic adaptability and tumor microenvironment interactions, highlighting BORIS and its downstream pathways as potential biomarkers and therapeutic targets in GBM.