@Article{biocell.2026.075061,
AUTHOR = {Gerardo Ramírez-Mejía, Sofía Plata-Burgos, Raquel Cuevas-Díaz Duran, Adrian Ledesma-Beiza, Cynthia Sámano, Thalía Estefanía Sánchez-Correa, Ernesto Soto-Reyes},
TITLE = {BORIS/<i>CTCFL</i> Reprograms Glioblastoma Transcriptional Networks through the Regulation of Tumor-Associated Genes such as <i>CD36</i> and <i>FBN2</i>},
JOURNAL = {BIOCELL},
VOLUME = {50},
YEAR = {2026},
NUMBER = {3},
PAGES = {--},
URL = {http://www.techscience.com/biocell/v50n3/66713},
ISSN = {1667-5746},
ABSTRACT = { <b>Objectives:</b> Glioblastoma multiforme (GBM) is a highly aggressive brain tumor characterized by extensive transcriptional and epigenetic dysregulation. Brother of the Regulator of Imprinted Sites (BORIS/CTCFL) has been implicated in oncogenic transcriptional programs in several cancers, but its role in GBM remains poorly defined. This study aimed to characterize BORIS-associated transcriptional programs in GBM and to assess their functional relevance using integrative computational and experimental approaches. <b>Methods:</b> Transcriptomic data from The Cancer Genome Atlas (TCGA)-GBM and Genotype-Tissue Expression (GTex) brain cortex were analyzed following batch correction, differential expression analysis, and gene ontology enrichment. TCGA-GBM samples were stratified into BORIS-high and BORIS-low expression quartiles to identify BORIS-associated gene signatures. BORIS chromatin occupancy was examined by Chromatin immunoprecipitation combined with sequencing (ChIP-seq) in U87MG cells, followed by functional annotation of BORIS-bound genes. Experimental validation included BORIS overexpression, RT-qPCR, immunoblotting, ChIP-qPCR, and functional assays assessing proliferation, clonogenic survival, and migration. <b>Results:</b> BORIS was significantly upregulated in GBM compared with normal brain tissue and was associated with transcriptional programs related to development, metabolism, and cell signaling. Quartile-based analysis identified BORIS-associated differentially expressed genes, including <i>CD36</i> and <i>FBN2</i>. ChIP-seq revealed BORIS binding at promoter-proximal regions, with ChIP-qPCR confirming occupancy at <i>CD36</i> and <i>FBN2</i> regulatory regions. BORIS overexpression increased <i>CD36</i> and <i>FBN2</i> expression and was associated with reduced proliferation, enhanced clonogenic survival, and increased migratory capacity. <b>Conclusion:</b> These findings indicate that BORIS is associated with transcriptional and phenotypic programs linked to GBM aggressiveness and may represent a candidate for further investigation as a biomarker or therapeutic target in GBM.},
DOI = {10.32604/biocell.2026.075061}
}