Similar Datasets
Project description:P53 mutation is closely associated with the occurrence and progression of colon cancer. In this project, we did crotonylomics sequencing by using human colon cancer homologous cell line pair-HCT116+/+(with wild type p53) and HCT116-/- (with null p53). Crotonylomics sequencing results showed that p53 deficiency regulated crotonylation of non-histone proteins.
2024-05-22 | PXD047258 | Pride
Project description:sequencing data in multiple cell lines
| PRJNA849415 | ENA
Project description: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.
| S-EPMC7772531 | biostudies-literature
Project description:Caco-2 and HT-29 cells were barcoded using the CloneTracker lentiviral barcode library and then irinotecan and capecitabine resistant derivatives of these cell lines were established. Four million barcoded Caco-2 and HT-29 cell were seeded into 15 cm cell culture dishes. When the cells reached confluency, two million cells per dish were seeded into four different 15 cm dishes with 25 mL medium (DMSO Control, Replica A, B, C) and two million cell pellets were stocked as initial cell population.For Caco-2 cell line, mediums in the dishes were changed twice a week with fresh mediums containing IC50 dose (4 months) and subsequently 2x IC50 dose (2 months) of capecitabine, for HT-29 cell line IC50 dose (6 months) of irinotecan. Caco-2 and HT-29 cell lines treated with DMSO were given the same amount of DMSO used in dissolving compounds as fresh medium. Following the end points of six months for each cell line, DNA isolation from harvested cell lines and collected medium of resistant B cell lines were carried out and barcodes were sequenced.
2023-07-11 | E-MTAB-12818 | biostudies-arrayexpress
Project description:BackgroundThe integration of human papillomavirus (HPV) is closely related to the occurrence of cervical cancer. However, little is known about the complete state of HPV integration into the host genome.MethodsIn this study, three HPV-positive cell lines, HeLa, SiHa, and CaSki, were subjected to NANOPORE long-read sequencing to detect HPV integration. Analysis of viral integration patterns using independently developed software (HPV-TSD) yielded multiple complete integration patterns for the three HPV cell lines.ResultsWe found distinct differences between the integration patterns of HPV18 and HPV16. Furthermore, the integration characteristics of the viruses were significantly different, even though they all belonged to HPV16 integration. The HPV integration in the CaSki cells was relatively complex. The HPV18 integration status in HeLa cells was the dominant, whereas the percentage of integrated HPV 16 in SiHa and CaSki cells was significantly lower. In addition, the virus sequences in the HeLa cells were incomplete and existed in an integrated state. We also identified a large number of tandem repeats in HPV16 and HPV18 integration. Our study not only clarified the feasibility of high-throughput long-read sequencing in the study of HPV integration, but also explored a variety of HPV integration models, and confirmed that viral integration is an important form of HPV in cell lines.ConclusionElucidating HPV integration patterns will provide critical guidance for developing a detection algorithm for HPV integration, as well as the application of virus integration in clinical practice and drug research and development.
| S-EPMC10758443 | biostudies-literature
Project description:MicroRNA sequencing of non-seminomatous germ cell tumor cell lines of yolk-sac tumor (YST) and embryonal carcinoma (EC) origin.
2025-01-01 | GSE254140 | GEO
Project description:We performed genome-wide DNA methylation profiling of KMS11, MM.1S, and RPMI8226 multiple myeloma cell lines to identify methylation changes distinct to each cell line
2015-06-30 | GSE68259 | GEO
Project description:We performed Illumina Infinium whole-genome SNP-CN profiling of KMS11, MM.1S, and RPMI8226 multiple myeloma cell lines to detect gene copy number variants distinct to each cell line
2015-06-30 | GSE68258 | GEO
Project description:Beginning with precursor lesions, aberrant DNA methylation marks the entire spectrum of prostate cancer progression. We mapped the global DNA methylation patterns in prostate tissues (n=17) and cells (n=2) from fifty nanograms of genomic DNA using Methylplex-Next Generation Sequencing (M-NGS). A Hidden Markov Model (HMM)-based algorithm previously used for Chip-Seq data analysis(http://www.sph.umich.edu/csg/qin/HPeak) was used to locate peaks from mapped reads obtained in each sequencing run. The total methylation events in intergenic/intronic regions between benign adjacent and cancer tissues were comparable. While approximately 20% of all CpG islands (CGIs) (68,508) were methylated in tissues, promoter CGI methylation gradually increased from ~12.6% in benign samples to 19.3% and 21.8% in localized and metastatic cancer tissues. We found distinct patterns in promoter methylation around transcription start sites, where methylation occurred directly on the CGIs, flanking regions and on CGI sparse promoters. Among the 6,691 methylated promoters in prostate tissues, 2481 differentially methylated regions (DMRs) are cancer specific and several previously studied targets were among them. A novel cancer specific DMR in WFDC2 promoter showed 77% methylation in cancer (17/22), 100% methylation in transformed prostate cell lines (6/6), none in the benign tissues (0/10) and normal PrEC cells. Integration of LNCaP DNA methylation and H3K4me3 data suggested a role for DNA methylation in alternate transcription start site utilization. While methylated promoters containing CGIs had mutually exclusive H3K4me3 modification, the histone mark was absent in CGI sparse promoters. Finally, we observed difference in methylation of LINE-1 elements between transcription factor ERG positive and negative cancers. The comprehensive methylome map presented here will further our understanding of epigenetic regulation of the prostate cancer genome. We mapped the global DNA methylation patterns in prostate tissues (n=17; data not available in GEO - being deposited in dbGaP for controlled access) and cells (n=2) from fifty nanograms of genomic DNA using Methylplex-Next Generation Sequencing (M-NGS). For replicate analysis in cell lines, a total of 4 runs were completed for PrEC prostate normal cell line, and 5 runs were completed for LNCaP prostate cancer cell line. For tissue samples, 2 benign prostate samples were ran twice on illumina next generation sequencing platform to access overall repeatability of M-NGS.
2011-05-09 | E-GEOD-27618 | biostudies-arrayexpress
Project description:Transcript sequencing data in BT549 cell line.
| PRJNA1139676 | ENA