Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA123867 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Multi-component epigenetic control of pro-invasive genes in cancer cells
| PRJNA121305 | ENA
Project description:Multi-component epigenetic control of pro-invasive genes in cancer cells (miRNA)
| PRJNA123871 | ENA
Project description:Multi-component epigenetic control of pro-invasive genes in cancer cells (ChIP-chip)
| PRJNA123869 | ENA
Project description:Epigenetic regulators have emerged as critical factors governing the biology of cancer. Here, in the context of melanoma, we show that RNF2 is prognostic, exhibiting progression-correlated expression in human melanocytic neoplasms. Through a series of gain of function and loss of function studies, we establish that RNF2 is oncogenic and pro-metastatic. Mechanistically, RNF2-mediated invasive behavior is dependent on its ability to mono-ubiquitinate H2AK119 at the promoter of LTBP2, resulting in silencing of this negative regulator of TGFβ signaling. In contrast, RNF2's oncogenic activity did not require its catalytic activity nor derives from its canonical gene repression function, rather RNF2 drives proliferation through direct transcriptional up-regulation of the cell cycle regulator CCND2. In summary, RNF2 regulates distinct biological processes in the genesis and progression of melanoma via distinct molecular mechanisms, underscoring the complex and multi-faceted actions of epigenetic regulators in cancer. RNF2 is overexpressed in immortalized human melanocytes HMEL-BRAFV600E to address impact of RNF2 overexpression in melanoma. GFP was overexpressed in HMEL-BRAFV600E cells as a control cell line. Expression profiling using microarray was performed and compared between RNF2 overexpressing versus GFP overexpressing HMEL-BRAFV600E cells.
2016-07-03 | E-GEOD-51928 | biostudies-arrayexpress
Project description:Epigenetic regulators have emerged as critical factors governing the biology of cancer. Here, in the context of melanoma, we show that RNF2 is prognostic, exhibiting progression-correlated expression in human melanocytic neoplasms. Through a series of gain of function and loss of function studies, we establish that RNF2 is oncogenic and pro-metastatic. Mechanistically, RNF2-mediated invasive behavior is dependent on its ability to mono-ubiquitinate H2AK119 at the promoter of LTBP2, resulting in silencing of this negative regulator of TGFβ signaling. In contrast, RNF2's oncogenic activity did not require its catalytic activity nor derives from its canonical gene repression function, rather RNF2 drives proliferation through direct transcriptional up-regulation of the cell cycle regulator CCND2. In summary, RNF2 regulates distinct biological processes in the genesis and progression of melanoma via distinct molecular mechanisms, underscoring the complex and multi-faceted actions of epigenetic regulators in cancer. RNF2 is overexpressed in immortalized human melanocytes HMEL-BRAFV600E to address impact of RNF2 overexpression in melanoma and identify RNF2 target genes. ChIP was performed to identify RNF2 binding sites using antibody against the V5 tag.
2016-07-03 | E-GEOD-51929 | biostudies-arrayexpress
Project description:To identify the epigenetic signature that controls cancer cell migration, we performed integrated gene expression, miRNA and epigenetic profiling of 486 selected invasion-associated genes in non-migratory MCF-7 breast carcinoma and highly migratory U251 glioma cells. We used a custom-built chromatin immunoprecipitation (ChIP)-on-Chip microarray that included complimentary oligonucleotide probes for the genes that were functionally linked to proteolysis, migration and tumorigenesis such as extracellular matrix proteins, cellular proteinases and their inhibitors, growth factors and cytokines, and adhesion and signaling receptors. As a result, we determined the role histone H3 modifications [(Lys-4 dimethylation (H3K4me2), Lys-27 trimethylation (H3K27me3) and acetylation (H3ac)] play in transcriptional regulation of the multiple invasion-associated genes. Predominantly, transcriptional silencing of the pro-invasive genes in MCF-7 cells involved the repressive H3K27me3 mark and, frequently, the presence of the stem cell-like bivalent epigenetic mark (enrichment in both H3K27me3 and H3K4me2). In turn, pro-invasive genes in U251 cells were epigenetically stimulated by a gain in H3K4me2 and histone H3 hyperacetylation, and by a global reduction of H3K27me3. Intriguingly, the expression of multiple collagen genes was highly enhanced in glioma cells, thus suggesting that gliomas themselves deposit a specialized, invasion-promoting matrix. Microarray probes were designed using eArray software (Agilent). Unique DNA probes specific to 486 human genes from the high density (HD) ChIP Database (Agilent) were included in each microarray. Microarray, 8x15K format, slides were custom manufactured by Agilent. Additional hybridization control probes (universal control grid LA577) were included in the arrays (Agilent). Each individual probe in the microarray was replicated 3-10 times. MCF7 vs.U251 cells
2010-05-16 | E-GEOD-18890 | biostudies-arrayexpress
Project description:To identify the epigenetic signature that controls cancer cell migration, we performed integrated gene expression, miRNA and epigenetic profiling of 486 selected invasion-associated genes in non-migratory MCF-7 breast carcinoma and highly migratory U251 glioma cells. We used a custom-built chromatin immunoprecipitation (ChIP)-on-Chip microarray that included complimentary oligonucleotide probes for the genes that were functionally linked to proteolysis, migration and tumorigenesis such as extracellular matrix proteins, cellular proteinases and their inhibitors, growth factors and cytokines, and adhesion and signaling receptors. As a result, we determined the role histone H3 modifications [(Lys-4 dimethylation (H3K4me2), Lys-27 trimethylation (H3K27me3) and acetylation (H3ac)] play in transcriptional regulation of the multiple invasion-associated genes. Predominantly, transcriptional silencing of the pro-invasive genes in MCF-7 cells involved the repressive H3K27me3 mark and, frequently, the presence of the stem cell-like bivalent epigenetic mark (enrichment in both H3K27me3 and H3K4me2). In turn, pro-invasive genes in U251 cells were epigenetically stimulated by a gain in H3K4me2 and histone H3 hyperacetylation, and by a global reduction of H3K27me3. Intriguingly, the expression of multiple collagen genes was highly enhanced in glioma cells, thus suggesting that gliomas themselves deposit a specialized, invasion-promoting matrix. miRNA global profiling complements the ChIP-on-Chip experiment with U251 and MCF-7 cells. Two-condition experiment, MCF7 vs.U251 cells. 2 Biological replicates for each cell line
2010-01-05 | E-GEOD-18894 | biostudies-arrayexpress
Project description:Here we present a functional multi-omics method, interaction-Correlated Multi-omic Aberration Patterning or iC-MAP, which dissects intra-tumor heterogeneity and identifies in situ in real time the oncogenic consequences of multi-omics aberrations that drive proliferative/invasive tumor in individuals with poor prognosis. First, given epigenetic aberrations resulting from complex interactions between genetic susceptibility and environmental influences are the primary driving force of tumorigenesis, we applied our chromatin activity-based chemoproteomics (ChaC) method to characterize the tumor-phenotypic epiproteomes (epigenetic regulatory proteomes) in breast cancer (BC) patient tissues. A biotinylated ChaC probe UNC0965 that specifically binds to the oncogenically active histone methyltransferase G9a enabled the sorting/enrichment of a G9a-interacting epiproteome representing the predominant BC subtype in a tissue, which is separated from other cell types, especially non-malignant cells where G9a is less enzymatically active. ChaC then identified UNC0965-captured G9a interactors that are mostly involved in the oncogenic pathways associated with tumor cell viability and invasion. Using BC patient transcriptomic/genomic data we retrospectively identified the G9a interactor-encoding genes that show individualized iC-MAP in BC-subtypic patients with incurable metastatic disease, revealing essential drivers of proliferative or invasive BC phenotypes. Our iC-MAP findings can not only act as new diagnostic/prognostic markers to identify patient subsets with metastatic disease but also create precision therapeutic strategies that can match proliferative or invasive potential of individual patients.
2019-07-26 | PXD013795 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE17768: An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: gene expression GSE17769: An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: DNA methylation GSE21347: An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: allelic status GSE21540: An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: CGH Refer to individual Series
2010-12-31 | E-GEOD-21541 | biostudies-arrayexpress
Project description:A novel role of the actin cytoskeleton regulatory protein hMENA in the reciprocal pro-invasive interaction between cancer associated fibroblasts and cancer cells via Axl-Gas6 pathway
2019-12-13 | MSV000084685 | MassIVE