biostudies-arrayexpressGerardo Ramirez-MejiaHomo sapienshttps://www.ebi.ac.uk/biostudies/studies/E-MTAB-15935Glioblastoma multiforme (GBM) remains one of the most aggressive and lethal brain tumors. BORIS (CTCFL) functions as an epigenetic and transcriptional regulator implicated in multiple cancers; however, its role in GBM is poorly understood. To explore its regulatory function, we performed ChIP-seq profiling in U87MG cells.biostudies-arrayexpressSample Collection - U87MG cells ~70% confluence. Cross-link: 1% formaldehyde (stock buffer: 11% formaldehyde, 100 mM NaCl, 0.5 mM EGTA, 50 mM HEPES), quenched with glycine (final 125 mM), lysed (50 mM Tris-HCl, 150 mM NaCl, 1% NP-40, supplemented with cOmplete ™ protease inhibitor Cocktail), and sonicated.Nucleic Acid Extraction - Immunoselected DNA was purified using MinElute columns (Qiagen, 28204).Sample Treatment - Raw reads were quality checked and timed using Trimmomatic to remove adapters and low-quality bases.Sequencing - Performer: CDGenomics. Using standard ChIP-seq library preparation for Illumina NovaSeq 6000 PE150 platformLibrary Construction - Sequencing performed by CDGenomics using standard ChIP-seq library preparation for Illumina NovaSeq 6000Growth Protocol - D-MEM/F-12 medium supplemented with 29 mM sodium bicarbonate, adjusted to pH 7.4, and sterilized using a 0.2 μm pore size filter unit. The medium was further supplemented with 10% heat inactivated fetal bovine serum. Cells were maintained at 37 °C in a humidified incubator with 5% CO2.OrganizationMINSEQE ScoreAssays and DataProcessed DataMAGE-TAB FilesSequence Alignment - Clean reads were aligned to the human reference genome (GRCh38) using BWA-MEM. Aligned files were processed with Picard to mark and remove PCR duplicates, and SAMtools was used for sorting and indexing. Peak calling was performed with MACS2 using default parameters. BigWig coverage tracks were generated with deepTools for visualization. Peak annotation and genomic feature enrichment analyses were conducted using the ChIPseeker R package. BigWig coverage tracks were generated with deepTools for visualization. Peak annotation and genomic feature enrichment analyses were conducted using the ChIPseeker R packageData Transformation - Aligned files were processed with Picard to mark and remove PCR duplicates, and SAMtools was used for sorting and indexing.MetabolomicsUnknownTranscriptomicsGenomicsProteomicsIllumina NovaSeq 6000ChIP-seqHomo sapiensBORIS/CTCFL Reprograms Glioblastoma Transcriptional Networks through the Regulation of Tumor-Associated Genes such as CD36 and FBN2Gerardo Ramirez-MejiaGerardo Ramírez-Mejía, Sofía Plata-Burgos, Raquel Cuevas-Díaz Duran, Adrian Ledesma-Beiza, Cynthia Sámano, Thalía Estefanía Sánchez-Correa, Ernesto Soto-ReyesfalseBORIS/CTCFL reprograms glioblastoma transcriptional networks through regulation of tumor-associated genes such as CD36 and FBN2Glioblastoma multiforme (GBM) remains one of the most aggressive and lethal brain tumors. BORIS (CTCFL) functions as an epigenetic and transcriptional regulator implicated in multiple cancers; however, its role in GBM is poorly understood. To explore its regulatory function, we performed ChIP-seq profiling in U87MG cells.2026-01-30T00:00:00Z2026-05-27T14:46:26.188Z2025-10-23T15:08:05.853ZE-MTAB-15935ERP182608EFO_0002944EFO_0004170EFO_0003789EFO_0002692EFO_0004917EFO_0005518EFO_0003816EFO_0004184EFO_000396910.32604/biocell.2026.075061