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Epigenome analysis of HDAC1 stably knocked down HCT116 cells and HCT116 cells stably expressing UHRF1 mutant

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE151865 | GEO | 2020/06/06

REPOSITORIES: GEO

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Epigenome analysis of HDAC1 stably knocked down HCT116 cells and HCT116 cells stably expressing UHRF1 mutant

Project description:Epigenome analysis of HDAC1 stably knocked down HCT116 cells and HCT116 cells stably expressing UHRF1 mutant

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Epigenome analysis of HDAC1 stably knocked down HCT116 cell [Illumina EPIC]

Project description:UHRF1 is a key regulator of DNA methylation maintenance. In this study, we investigated whether acetylation of UHRF1 affects its hemimethylated DNA binding affinity and alters genome-wide DNA methylation pattern. We observed that acetylation of UHRF1 is regulated by HDAC1 and PCAF. We investigated DNA methylation profile of HDAC1 depleted HCT116 cell with control cell.

2020-06-06 | GSE151861 | GEO

Epigenome analyses of HCT116 cells stably expressing UHRF1 mutant [Illumina EPIC]

Project description:UHRF1 is a key regulator of DNA methylation maintenance. In this study, we investigated whether acetylation of UHRF1 affects its hemimethylated DNA binding affinity and alters genome-wide DNA methylation pattern. We show that cells with mutation in K490 of UHRF1 have distinct methylation profile versus wildtype UHRF1 expressing cells.

2020-06-06 | GSE151862 | GEO

Epigenome analysis of HDAC1 stably knocked down HCT116 cell [Illumina EPIC]

Project description:Epigenome analysis of HDAC1 stably knocked down HCT116 cell [Illumina EPIC]

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Epigenome analyses of HCT116 cells stably expressing UHRF1 mutant [Illumina EPIC]

Project description:Epigenome analyses of HCT116 cells stably expressing UHRF1 mutant [Illumina EPIC]

| PRJNA637514 | ENA

Epigenome analysis of ALKBH5 knocked down HCT116 cell

Project description:ALKBH5 is one of the important m6A demethylases and is reported to be closely associated with tumorigenesis.In this study, we investigated whether ALKBH5 could affect genome-wide DNA methylation pattern. We investigated DNA methylation profile of ALKBH5 deleted HCT116 cell with control cell. The Illumina Infinium HumanMethylation 850K BeadChip was used. Samples included 2 HCT1116 shNC and 4 HCT116 shALKBH5.

2024-12-07 | GSE190375 | GEO

Epigenome analysis of ALKBH5 knocked down HCT116 cell

Project description:Epigenome analysis of ALKBH5 knocked down HCT116 cell

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Gene amplification in human cells knocked down for RAD54.

Project description:BackgroundIn mammalian cells gene amplification is a common manifestation of genome instability promoted by DNA double-strand breaks (DSBs). The repair of DSBs mainly occurs through two mechanisms: non-homologous end-joining (NHEJ) and homologous recombination (HR). We previously showed that defects in the repair of DSBs via NHEJ could increase the frequency of gene amplification. In this paper we explored whether a single or a combined defect in DSBs repair pathways can affect gene amplification.ResultsWe constructed human cell lines in which the expression of RAD54 and/or DNA-PKcs was constitutively knocked-down by RNA interference. We analyzed their radiosensitivity and their capacity to generate amplified DNA. Our results showed that both RAD54 and DNA-PKcs deficient cells are hypersensitive to γ-irradiation and generate methotrexate resistant colonies at a higher frequency compared to the proficient cell lines. In addition, the analysis of the cytogenetic organization of the amplicons revealed that isochromosome formation is a prevalent mechanism responsible for copy number increase in RAD54 defective cells.ConclusionsDefects in the DSBs repair mechanisms can influence the organization of amplified DNA. The high frequency of isochromosome formation in cells deficient for RAD54 suggests that homologous recombination proteins might play a role in preventing rearrangements at the centromeres.

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Down-regulation of UCRP and UBE2L6 in BRCA2 knocked-down human breast cells.

Project description:To understand the effects of the transient ablation of BRCA2 gene expression in dividing human breast cells, we transiently knocked down BRCA2 mRNA in HMEC and other cells. Microarray analysis of mRNAs revealed the down-regulation of the mRNAs of ubiquitin cross-reacting protein (UCRP) and the E2 enzyme that help conjugating UCRP to its target proteins, namely UBE2L6 (UbcH8), in BRCA2 ablated cells. UCRP is an interferon regulated protein, involved in cell growth and cell cycle events by participating in the degradation/modulation of cell cycle regulatory proteins. Quantitative-PCR and Northern analysis confirmed down-regulation of UCRP and UBE2L6 with BRCA2 knockdown, respectively. Since UCRP and UCRPylation have critical roles in the innate immunity against viral infection and during pregnancy, our observation may indicate new roles of the BRCA2 protein.

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HDAC1-mSin3a-NCOR1, Dnmt3b-HDAC1-Egr1 and Dnmt1-PCNA-UHRF1-G9a regulate the NY-ESO1 gene expression.

Project description:The NY-ESO1 gene is a cancer/testis antigen considered to be suitable target for the immunotherapy of human malignancies. Despite the identification of the epigenetical silencing of the NY-ESO1 gene in a large variety of tumors, the molecular mechanism involved in this phenomenon is not fully elucidated. In two non epithelial cancers (glioma and mesothelioma), we found that the epigenetic regulation of the NY-ESO1 gene requires the sequential recruitment of the HDAC1-mSin3a-NCOR, Dnmt3b-HDAC1-Egr1 and Dnmt1-PCNA-UHRF1-G9a complexes. Thus, our data illustrate the orchestration of a sequential epigenetic mechanism including the histone deacetylation and methylation, and the DNA methylation processes.

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