| dc.description.abstract | Astrocytomas are the most common and aggressive type of primary brain tumors in adults. The World Health Organization (WHO) assorts them into grades, from I to IV, based on histopathological features that reflect their malignancy [1]. Alongside with tumor progression, comes an increased proliferation, genomic instability, infiltration in normal brain tissue and resistance to treatments. The high genomic instability forges tumor cells enhancing key proteins that avoid cells from collapsing and favor therapy resistance [2]. To explore genes and pathways associated with tumor progression phenotypes we analyzed gene expression in a panel of non-tumor and glioma cell lines, namely: ACBRI371, non-tumor human astrocytes; HDPC, fibroblasts derived from dental pulp; Res186, Res259, Res286 and UW467 that include grade I, II and III astrocytoma cell lines derived from pediatric tumors; and T98G, U343MG, U87MG, U138MG and U251MG, all derived from GBM (grade IV). We also profiled gene expression changes caused by exogenously induced replicative stress, performing RNA sequencing with camptothecin (CPT)-treated cells. Here we describe the RNA-sequencing data set acquired, including quality of reads and sequencing consistency, as well as the bioinformatics strategy used to analyze it. We also compared gene expression patterns and pathway enrichment between non-tumor versus lower-grade (LGG), non-tumor versus GBM, LGG versus GBM, and CPT-treated versus non-treated cells. In brief, a total of 6467 genes showed differential expression and 5 pathways were enriched in tumor progression, while 2279 genes and 7 pathways were altered under the replication stress condition. The raw data was deposited in the NCBI BioProject database under the accession number PRJNA631805. Our dataset is valuable for researchers interested in differential gene expression among different astrocytoma grades and in expression changes caused by replicative stress, facilitating studies that seek novel biomarkers of glioma progression and treatment resistance. | |
