Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Trancriptomic profiling of HCT116 colon cancer cells with or without PBRM1 knock-down by RNAi

ABSTRACT: Trancriptomic profiling of HCT116 colon cancer cells with or without PBRM1 knock-down by RNAi

PROVIDER: PRJEB19980 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR1880961.fastq.gz	Fastqsanger.gz
	ERR1880962.fastq.gz	Fastqsanger.gz
	ERR1880963.fastq.gz	Fastqsanger.gz
	ERR1880964.fastq.gz	Fastqsanger.gz
	ERR1880965.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Trancriptomic profiling of HCT116 colon cancer cells with or without PBRM1 knock-down by RNAi

Project description:To investigate the influence of PBRM1 on gene expression, we performed RNA-seq in HCT116 colon cancer cells with or without PBRM1 knock-down by RNAi (both shRNA and siRNA approaches were used), and identified differentially expressed genes in PBRM1 knock-down cells compared to control cells, which shows implications for PBRM1's biological function in colon cancer.

2018-01-30 | E-MTAB-5566 | biostudies-arrayexpress

PBRM1 Knockdown in RCC Cell Lines

Project description:PBRM1 was found to be mutated in a high percentage of clear cell RCCs. We performed knockdown of PBRM1 via siRNA and compared with scrambled control in three different RCC cell lines. PBRM1 siRNA and mock treated cell lines were normalized together with 'hypoxic' clear cell renal tumors and normal renal tissue samples from GSE17818.

2011-01-20 | E-GEOD-22316 | biostudies-arrayexpress

PBRM1 deficiency is synthetic lethal with PARP inhibitors in human cancers

Project description:Polybromo-1 (PBRM1), which encodes a specific subunit of the pBAF chromatin remodeling complex, is inactivated in multiple malignancies including 50% of clear cell renal cell carcinoma. At present, a therapeutic strategy that selectively targets PBRM1 defects does not exist. PBRM1 is involved in multiple cellular processes including transcription, replication and DNA repair. Using high-throughput screens and multiple isogenic and non-isogenic models, we found that PBRM1 defects cause synthetic lethality with several clinical PARP inhibitors, both in vitro and in vivo. This effect was enhanced using combinations with either small molecule ATR or BET inhibitors. Mechanistically, PBRM1 defects caused increased replication stress, R-loop formation and genomic instability that was exacerbated by PARP inhibitors. We also found that PARP and ATR inhibitors activate the cGAS-STING innate immunity pathway in PBRM1-deficient but not in PBRM1-proficient cells. These data provide the pre-clinical rationale for assessing PARP inhibitors as a monotherapy or in combination with ATR inhibitors or immune checkpoint inhibitors, in patients with PBRM1-deficient cancers.

2022-02-21 | PXD017826 | Pride

Expression of p27 target genes in WT HCT116 cells vs shPCAF knock down cells

Project description:We analyzed the transcriptional programs regulated by PCAF and p27 in the colon cancer cell line HCT116 by ChIP-seq. PCAF or p27 knock down revealed that both regulated the expression of common genes. In this dataset, we include the expression data of 852 genes regulated by PCAF, obtained from the comparison between WT HCT116 cells and shPCAF knock down cells

2017-01-18 | GSE93694 | GEO

Genome wide analysis of transcriptome modification after re-expression of PBRM1 WT and its BAH domain mutant in PBRM1 CRISPR-KO HEK293T cells.

Project description:Purpose: To find out if cancer-associated mutation in BAH domain affects gene expression? Method: We used PBRM1 CRISPR KO HEK293T cells and ectopically expressed GFP-PBRM1-WT, GFP-PBRM1 P1048R, GFP-PBRM1 T1202K and GFP-PBRM1 C1233W plasmid for 48 hours. Result: We found that GFP-PBRM1 WT and GFP-PBRM1 T1202K mutant were identical in terms of gene expression. However, mutant P1048R and C1233W had very little difference in expression of only 15 (14 up- and 1 down) out of 10,160 genes.

2021-09-20 | GSE149874 | GEO

Genome-wide chromatin profiles of PBRM1 [RNA-Seq]

Project description:PBRM1 is an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler. The inactivation of PBRM1 is the second most frequent mutational event in kidney tumorigenesis. Here we show that in VHL-deficient ccRCC tumors, PBRM1 loss results in an altered PBAF complex that retains the association between SMARCA4 and ARID2 but disengages BRD7 from SMARCA4. The PBRM1-deficient PBAF complexes redistribute from promoter proxy regions to distal enhancer regions. The ATPase function of SMARCA4 enhances the recruitment of nuclear factor RELA to aberrant sites and promotes NF-κB activity. Proteasome inhibitor bortezomib reverses NF-κB activation by reducing RELA binding at regions bound by PBRM1-deficient PBAF and delays PBRM1-deficient tumor growth. In conclusion, PBRM1 safeguards the chromatin by repressing aberrant liberation of pro-tumorigenic NF-κB target genes by residual PBRM1-deficient PBAF complexes.

2023-02-13 | GSE152734 | GEO

Genome-wide chromatin profiles of PBRM1 [ChIP-Seq]

Project description:PBRM1 encodes an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler and the inactivation of PBRM1 is the second most frequent mutational event in kidney cancer. However, the impact of PBRM1 loss on chromatin remodeling, especially pertaining to kidney tumorigenesis, has not been well examined. Here we show that in VHL-deficient renal tumors, PBRM1 deficiency results in aberrant PBAF complexes that localize to de novo genomic loci and activate the pro-tumorigenic NF-?B pathway. PBRM1-deficient PBAF complexes, despite retaining the association between SMARCA4 and ARID2, have loosely tethered BRD7 and redistribute from promoter proximal regions to distal enhancers containing NF-?B motifs. Subsequently, PBRM1-deficient cells display heightened NF-?B activity in multiple models and clinical samples. The ATPase function of SMARCA4 maintains chromatin occupancy of both pre-existing and newly acquired RELA specific to PBRM1 loss, and activates downstream target gene expression. Proteasome inhibitor bortezomib reverses NF-?B activation by reducing RELA occupancy and delays growth of PBRM1-deficient tumors. In conclusion, PBRM1 safeguards the chromatin by repressing aberrant liberation of pro-tumorigenic NF-?B target genes by residual PBRM1-deficient PBAF complexes.

2023-02-13 | GSE152681 | GEO

RNAi knock down of mSin3a-b and SBTB4 in human colon carcinoma cell line HCT116

Project description:Efffects of silencing ZBTB4, mSin3a/mSin3b on HCT 116 human colon carcinoma cell lines for 48 hours

2008-03-31 | E-MEXP-1509 | biostudies-arrayexpress

PBRM1 Knockdown in RCC Cell Lines

2011-01-20 | GSE22316 | GEO

Comparing gene-expression profiles between control and CHD6 knock-down HCT116 cells

Project description:Colorectal cancer is one of the most common cancers. Cancer cells are highly dependent on dysregulated gene expression to support their uncontrolled growth and high energy needs. The expression of gene encoding chromodomain helicase DNA binding protein 6 (CHD6) is frequently altered in tumor tissues of colorectal cancer patients.We performed transcriptomic analysis to identify the differentially expressed genes between control and CHD6 KD HCT116.

2022-12-14 | GSE163124 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data