RNA sequencing data of different grade astrocytoma cell lines
Juliana Ferreira de Sousa,
Patrick da Silva,
Rodolfo Bortolozo Serafim,
Ricardo Perecin Nociti,
Cristiano Gallina Moreira,
Wilson Araujo Silva,
Valeria Valente
Affiliations
Juliana Ferreira de Sousa
Radiation Oncology Branch, National Cancer Institute, NIH, 10 Center Drive, Bethesda, MD 20892, United States
Patrick da Silva
Department of Clinical Analysis, School of Pharmaceutical Sciences, São Paulo State University (UNESP), Rodovia Araraquara-Jaú, Km 01 - s/n, Campos Ville, Araraquara, SP 14800-903, Brazil
Rodolfo Bortolozo Serafim
Department of Clinical Analysis, School of Pharmaceutical Sciences, São Paulo State University (UNESP), Rodovia Araraquara-Jaú, Km 01 - s/n, Campos Ville, Araraquara, SP 14800-903, Brazil; National Institute of Science and Technology in Stem Cell and Cell Therapy and Center for Cell-Based Therapy, Rua Tenente Catão Roxo, 2501, Monte Alegre, Ribeirão Preto, SP 14051-140, Brazil
Ricardo Perecin Nociti
National Institute of Science and Technology in Stem Cell and Cell Therapy and Center for Cell-Based Therapy, Rua Tenente Catão Roxo, 2501, Monte Alegre, Ribeirão Preto, SP 14051-140, Brazil; Department of Veterinary Medicine, Faculty of Animal Sciences and Food Engineering, University of São Paulo (USP), Av. Duque de Caxias Norte, 225, Campus Fernando Costa, 13635-900 Pirassununga, SP, Brazil
Cristiano Gallina Moreira
Department of Clinical Analysis, School of Pharmaceutical Sciences, São Paulo State University (UNESP), Rodovia Araraquara-Jaú, Km 01 - s/n, Campos Ville, Araraquara, SP 14800-903, Brazil
Wilson Araujo Silva
National Institute of Science and Technology in Stem Cell and Cell Therapy and Center for Cell-Based Therapy, Rua Tenente Catão Roxo, 2501, Monte Alegre, Ribeirão Preto, SP 14051-140, Brazil; Department of Genetics, Ribeirão Preto Medical School, University of São Paulo (USP), Avenida Bandeirantes, 3900, 14049-900 Ribeirão Preto, SP, Brazil; Center for Integrative Systems Biology, CISBi, NAP/USP, Rua Catão Roxo, 2501, Monte Alegre, Ribeirão Preto, SP 14051-140, Brazil
Valeria Valente
Department of Clinical Analysis, School of Pharmaceutical Sciences, São Paulo State University (UNESP), Rodovia Araraquara-Jaú, Km 01 - s/n, Campos Ville, Araraquara, SP 14800-903, Brazil; National Institute of Science and Technology in Stem Cell and Cell Therapy and Center for Cell-Based Therapy, Rua Tenente Catão Roxo, 2501, Monte Alegre, Ribeirão Preto, SP 14051-140, Brazil; Corresponding author at: Department of Clinical Analysis, School of Pharmaceutical Sciences, São Paulo State University (UNESP), Rodovia Araraquara-Jaú, Km 01 - s/n, Campos Ville, Araraquara, SP 14800-903, Brazil.
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.
