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Expression changes in Setdb1-knockdown with shRNA in Hepa1-6 cells, a mouse hepatocellular carcinoma line

ABSTRACT: Expression changes in Setdb1-knockdown with shRNA in Hepa1-6 cells, a mouse hepatocellular carcinoma line

PROVIDER: PRJNA1068985 | ENA |

REPOSITORIES: ENA

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Expression changes in Setdb1-knockdown with shRNA in Hepa1-6 cells, a mouse hepatocellular carcinoma line

Project description:SETDB1 is an epigenetic regulator via H3K9me3. Much is not known about the role of SETDB1 in hepatocellular carcinoma. In this study, we established an shRNA-based Setdb1-knockdown strain in the mouse hepatocellular carcinoma line Hepa1-6 and performed RNA sequencing to identify genes regulated by Setdb1.

2024-12-08 | GSE254197 | GEO

Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Project description:Purpose: The aim of this study is (1) to identify the chromatin occupancy of the epigenetic regulator Setdb1 in mouse embryonic fibroblasts (MEF); (2) to profile key epigenetic marks H3K9me2, H3K9me3 and H3K27me3; utilizing wildtype cells with nonsilencing shRNA mediated knockdown and Setdb1 geneTrap heterozygous cells with Setdb1 shRNA mediated knockdown. Methods: Chromatin immunoprecipitation for Setdb1, H3K9me2, H3K9me3 and H3K27me3 was performed essentially as in (Nelson et al. 2006). Briefly, nuclei were isolated from formaldehyde crosslinked MEFs and chromatin was fragmented by sonication. Chromatin immunoprecipitation was performed with corresponding antibodies for Setdb1, H3K9me2, H3K9me3 and H3K27me3. DNA was extracted from the immunoprecipitated fraction following reverse-crosslinking. Isolated DNA was used to generate sequencing libraries with Illumina's TruSeq DNA Sample Preparation Kit according to manufacturer's instruction. Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads. Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data. Chromatin occupancy of the epigenetic regulator Setdb1, H3K9me2, H3K9me3 and H3K27me3 in mouse embryonic fibroblasts (MEFs) with wildtype MEFs and nonsilencing shRNA mediated knockdown or Setdb1 geneTrap heterozygous MEFs with Setdb1 shRNA mediated knockdown was determined by Setdb1, H3K9me2, H3K9me3 and H3K27me3 ChIP-seq, respectively.

2016-05-18 | E-GEOD-66522 | biostudies-arrayexpress

Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Project description:Purpose: The aim of this study was to determine the DNA methylation state of wildtype female mouse embryonic fibroblasts with nonsilencing shRNA mediated knockdown and Setdb1 geneTrap heterozygous cells with Setdb1 shRNA mediated knockdown. Methods: Enhanced Reduced Representation Bisulfite Libraries (eRRBS) were produced as previously descirbed (Akalin et al. 2012). Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads with dark cycle parameters (Boyle et al. 2012). Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data. Determine the DNA methylation state of mouse embryonic fibroblasts (MEFs) with wildtype MEFs and nonsilencing shRNA mediated knockdown or Setdb1 geneTrap heterozygous MEFs with Setdb1 shRNA mediated knockdown. Single-end with dark cycle protocol (Boyle et al. 2012)

2016-05-18 | E-GEOD-66524 | biostudies-arrayexpress

E14 cells knockdown with shRNA

Project description:E14 cells knockdown with shRNA

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Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Project description:Purpose: The aim of this study was to profile the transcriptome of differentiating embryonic stem cells (ES) with nonsilencing shRNA mediated knockdown and Setdb1 geneTrap heterozygous cells with Setdb1 shRNA mediated knockdown. Methods: Female Setdb1+/+ XistâA/+ ES cells were induced to differentiate and RNA sampled on day 0, day 3 and day 5 of differentiation. RNAseq libraries were prepared with TruSeq RNA sample preparation v2 kit. Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads. Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data. Total RNA was extracted and purified from each cell type and their transcriptomes analysed by RNA-Seq.

2016-05-18 | E-GEOD-66523 | biostudies-arrayexpress

Transcriptome profiling of HCT116 cells and HCT116 cells with knockdown of SETDB1 by RNA-sequencing

Project description:HCT116 is a colorectal cancer cell line. SETDB1 is an epigenetic modification factor responsible for catalyzing the histone modification H3K9me3. Transcription of SETDB1 gene is enriched in embryonic neural cells during vertebrate embryogenesis. SETDB1 is upregulated in cancer cells and promotes cancers. We found that knockdown of SETDB1 in HCT116 cells led to a neuronal-like differentiation phenotype.

2022-06-30 | GSE192372 | GEO

E14 cells knockdown with siRNA or shRNA

Project description:E14 cells knockdown with siRNA or shRNA

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c-Myc/BMI1 axis is essential for SETDB1-mediated breast tumorigenesis

Project description:Copy number gain/amplification of SETDB1 has been found in several human cancers, but the detailed oncogenic mechanism(s) of SETDB1 contributing to breast cancer remains largely unexplored. In this project, we analyzed the transcriptome of human breast cancer cell lines (MDA-MB-231 and MDA-MB-453) upon silencing of SETDB1 to explore the potential mechanism(s) underlying SETDB1 promoted breast cancer. In MDA-MB-231 cells, SETDB1 was silenced by shRNA-1. In MDA-MB-453 cells, SETDB1 was reduced by shRNA-3.

2018-05-01 | GSE108656 | GEO

Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Project description:Purpose: The aim of this study was to profile the transcriptome of differentiating embryonic stem cells (ES) with nonsilencing shRNA mediated knockdown and Setdb1 geneTrap heterozygous cells with Setdb1 shRNA mediated knockdown. Methods: Female Setdb1+/+ Xist∆A/+ ES cells were induced to differentiate and RNA sampled on day 0, day 3 and day 5 of differentiation. RNAseq libraries were prepared with TruSeq RNA sample preparation v2 kit. Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads. Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data.

2016-05-18 | GSE66523 | GEO

Transcriptome profiling of NE-4C cells and NE-4C cells with knockdown of Setdb1 by RNA-sequencing

Project description:NE-4C is a mouse neural stem cell line used for study of neuronal differentiation. Setdb1 is an epigenetic modification factor responsible for catalyzing the histone modification H3K9me3. Transcription of Setdb1 gene is enriched in embryonic neural cells during vertebrate embryogenesis. Setdb1 is upregulated in cancer cells and promotes cancers. We found that knockdown of Setdb1 in NE-4C cells led to neuronal differentiation.

2022-06-30 | GSE192373 | GEO

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