Similar Datasets
Project description:Genomic and transccriptomic landscape of two step malignant transformation process.
| PRJEB37468 | ENA
Project description:The mechanistic links between transcription factors and the epigenetic landscape, which coordinate the deregulation of gene networks during cell transformation are largely unknown. We used an isogenic model of stepwise tumorigenic transformation of human primary cells to monitor the progressive deregulation of gene networks upon immortalization and oncogene-induced transformation. By combining transcriptome and epigenome data for each step during transformation and by integrating transcription factor (TF) - target gene associations, we identified 142 TFs and 24 chromatin remodelers/modifiers (CRMs), which are preferentially associated with specific co-expression paths that originate from deregulated gene programming during tumorigenesis. These TFs are involved in the regulation of divers processes, including cell differentiation, immune response and establishment/modification of the epigenome. Unexpectedly, the analysis of chromatin state dynamics revealed patterns that distinguish groups of genes, which are not only co-regulated but also functionally related. Further decortication of TF targets enabled us to define potential key regulators of cell transformation, which are engaged in RNA metabolism and chromatin remodelling. Our study suggests a direct implication of CRMs in oncogene-induced tumorigenesis and identifies new CRMs involved in this process. This is the first comprehensive view of gene regulatory networks that are altered during the process of stepwise human cellular tumorigenesis in a virtually isogenic system. Examination of 4 different histone modifications marks and RNA PolII in all 3 cell lines of stepwise tumorigenesis model with biological replicates
2016-05-13 | E-GEOD-72532 | biostudies-arrayexpress
Project description:Azoxymethane (AOM) and dextran sulfate sodium (DSS) mice, as a classic model for the study of colorectal cancer, can completely simulate the inflammatory cancer transformation in the development of colorectal cancer.Although people have been trying to reveal the key mechanism of colorectal cancer transformation. But the current understanding of it is still not enough. In this study, we injected mice with AOM and then periodically treated them with DSS. The mice were made to develop tumors in the colon finally. In this process, we sampled the intestinal tissues of the mice at different time points, respectively, at the 0th week, 2nd week, 4th week, 7th week and 10th week after AOM injection. In order to fully describe the epigenetic pattern of colorectal cancer in AOM/DSS mice, especially the dynamic changes in the process of inflammatory cancer transformation. we generated the histone modification profile of 5 markers, including H3K27Ac (active enhancer), H3K4me1 (enhancer), H3K4me3 (promoter), H3K9me3 (heterochromatin) and H3K27me3 (multicomb suppression) across 5 time points (week-0, week-2, week-4, week-7, week-10). Genome-wide epigenetic analysis found that during the tumorigenesis process, enhancer chromatin state region increased. And functionally related to apoptosis and mitochondrial function. When detecting the dynamic changes of the signal intensity of H3K27ac, it was found that the enhanced enhancer signal-related genes were enriched in the inflammatory factor NFKB signaling pathway. It shows that in the process of inflammatory cancer transformation, H3K27ac are involved in inflammation and cell apoptosis, and play an important role in inflammatory cancer transformation.
2022-06-14 | GSE178144 | GEO
Project description:Determining the miRNA and mRNA expression profiles in HaCaT cells at early and late stages of arsenite exposure to reveal early and late changes in the HaCaT cells transformation process.
2018-01-23 | GSE97305 | GEO
Project description:Determining the miRNA and mRNA expression profiles in HaCaT cells at early and late stages of arsenite exposure to reveal early and late changes in the HaCaT cells transformation process.
2021-07-07 | GSE153057 | GEO
Project description:The mechanistic links between transcription factors and the epigenetic landscape, which coordinate the deregulation of gene networks during cell transformation are largely unknown. We used an isogenic model of stepwise tumorigenic transformation of human primary cells to monitor the progressive deregulation of gene networks upon immortalization and oncogene-induced transformation. By combining transcriptome and epigenome data for each step during transformation and by integrating transcription factor (TF) - target gene associations, we identified 142 TFs and 24 chromatin remodelers/modifiers (CRMs), which are preferentially associated with specific co-expression paths that originate from deregulated gene programming during tumorigenesis. These TFs are involved in the regulation of divers processes, including cell differentiation, immune response and establishment/modification of the epigenome. Unexpectedly, the analysis of chromatin state dynamics revealed patterns that distinguish groups of genes, which are not only co-regulated but also functionally related. Further decortication of TF targets enabled us to define potential key regulators of cell transformation, which are engaged in RNA metabolism and chromatin remodelling. Our study suggests a direct implication of CRMs in oncogene-induced tumorigenesis and identifies new CRMs involved in this process. This is the first comprehensive view of gene regulatory networks that are altered during the process of stepwise human cellular tumorigenesis in a virtually isogenic system.
2016-05-13 | GSE72532 | GEO
Project description:The mechanistic links between transcription factors and the epigenetic landscape, which coordinate the deregulation of gene networks during cell transformation are largely unknown. We used an isogenic model of stepwise tumorigenic transformation of human primary cells to monitor the progressive deregulation of gene networks upon immortalization and oncogene-induced transformation. By combining transcriptome and epigenome data for each step during transformation and by integrating transcription factor (TF) - target gene associations, we identified 142 TFs and 24 chromatin remodelers/modifiers (CRMs), which are preferentially associated with specific co-expression paths that originate from deregulated gene programming during tumorigenesis. These TFs are involved in the regulation of divers processes, including cell differentiation, immune response and establishment/modification of the epigenome. Unexpectedly, the analysis of chromatin state dynamics revealed patterns that distinguish groups of genes, which are not only co-regulated but also functionally related. Further decortication of TF targets enabled us to define potential key regulators of cell transformation, which are engaged in RNA metabolism and chromatin remodelling. Our study suggests a direct implication of CRMs in oncogene-induced tumorigenesis and identifies new CRMs involved in this process. This is the first comprehensive view of gene regulatory networks that are altered during the process of stepwise human cellular tumorigenesis in a virtually isogenic system.
2016-05-13 | GSE72531 | GEO
Project description:Agrobacterium tumefaciens-mediated genetic transformation has been routinely used in rice for more than a decade. However, the transformation efficiency of the indica rice variety is still unsatisfactory and much lower than that of japonica cultivars. Further improvement on the transformation efficiency lies in the genetic manipulation of the plant itself, which requires a better understanding of the underlying process accounting for the susceptibility of plant cells to Agrobacterium infection as well as the identification of plant genes involved in the transformation process. In order to investigate the related genes affecting the transformation efficiency of embryogenic calli of different rice cultivars, we used Affymetrix GeneChip® Rice Genome Array to measure the global gene expression profiling just before transformation and at four different time points after transformation (1 h, 6 h, 12 h, 24 h) in both japonica rice cultivar Nipponbare and indica rice cultivar Zhenshan 97.
2012-01-01 | GSE32426 | GEO
Project description:A growing number of studies describe multiple functions of lncRNAs in chromatin that support their active roles in normal and disease-specific gene expression. We identified a specific enhancer-associated LINC01116 (named HOXDeRNA), which targeted activation transformed human astrocytes into glioma-like cells. Using a combination of RNA-Seq, ChIRP-Seq, and ChIP-Seq, we defined the transcriptomic and epigenetic changes underlying the transformation. We demonstrate that HOXDeRNA binds in trans to the promoters of 44 glioma-specific transcription factors distributed throughout the genome and derepresses them by removing the Polycomb 2 complex. This process is mediated by the RNA G-quadruplex structure of HOXDeRNA. Moreover, HOXDeRNA-induced astrocyte transformation is accompanied by the activation of glioma-specific super-enhancers enriched for binding sites of glioma master transcription factors SOX2 and OLIG2, and multiple oncogenes such as EGFR, PDGFR, BRAF, and miR-21. Our results help reconstruct the sequence of events underlying the process of astrocyte transformation and suggest a driving role of HOXDeRNA eRNA in gliomagenesis.
2023-03-31 | GSE227803 | GEO
Project description:To understand transcriptome and epigenome profilings alteration during breast cancer initiation and development, we constructed a in vitro breast cancer transformation model. And then, we use mRNA-Seq to uncover differential expression genes during breast cancer transformation process. For epigenomic profilings, we specificly analysis genome wide H3K9me2, H3K9me3,H3K4me3 and H3K27me3 modifications using ChIP-Seq. We found that H3K9 di and tri methylation decrease both in vitro breast cancer cell transformation model and in vivo clinical samples. Further more, we found KDM3A, a demethylase for H3K9 mono and di methylation, increase during the breast cancer model transformation process and clinical samples. KDM3A deficiency impairs the growth of those transformed cell lines and its overexpression promotes tumor formation.
2016-04-08 | GSE64367 | GEO