Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BPTF Depletion Enhances NK Cell Mediated Antitumor Immunity

ABSTRACT: In mouse models, the bromodomain PHD finger transcription factor (BPTF) chromatin remodeling subunit in tumor cells suppresses natural killer (NK) cell antitumor activity. In vitro, BPTF suppresses NK cell cytolytic activity to mouse and human cancer cell lines, demonstrating a conserved function.

ORGANISM(S): Mus musculus

PROVIDER: GSE85756 | GEO | 2017/04/28

SECONDARY ACCESSION(S): PRJNA339273

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors

Project description:Purpose: Evaluation of the impact of a reduction in Bptf levels on the nature of lymphomas arising from Em-Myc mice. Results: Bptf heterozygous tumors show reduced activity of the E2F and c-MYC pathways, together with increased activity of the NF-kB pathway.

2019-12-10 | GSE141647 | GEO

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [RNA-Seq]

Project description:The c-MYC oncogene is a key transcription factor deregulated in most human tumors. Histone marks associated with transcriptionally active genes in euchromatic islands define the set of high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are not known but likely involve chromatin-remodelling and chromatin-modifying complexes. Here, we show that c-MYC interacts with BPTF, a core subunit of the NURF complex that binds active chromatin. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to a decrease in c-MYC recruitment to DNA and to changes in chromatin accessibility. Using BPTF-null MEFs we show that BPTF is necessary for c-MYC-driven proliferation, G1-S progression, and replication stress, but not for c-MYC-driven apoptosis. Consistently, BPTF is required for the proliferation of cells driven by c-MYC, such as Burkitt lymphoma, and its expression in human cancer lines correlates with the activation of c-MYC gene signatures. Our findings point to the c-MYC-BPTF axis as a potential therapeutic target in cancer. To assess whether BPTF is required for the transcriptional activity of c-MYC, human foreskin fibroblasts (HFF) were stably transduced with the chimeric MYC-ER cDNA (HFF MYC-ER) and infected with lentiviruses coding for either control (shNt) or BPTF-targeting shRNAs. Cells were serum-starved for 2 days to achieve quiescence and then treated with 4-hydroxytamoxifen (4-OHT)

2016-01-19 | E-GEOD-65545 | biostudies-arrayexpress

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [ChIP-Seq]

2016-01-19 | E-GEOD-65544 | biostudies-arrayexpress

Proteomic profiling of subsets of NK cell-derived extracellular vesicles by LC-MS/MS

Project description:In this study we have compared the proteomic profile of subsets of extracellular vesicles (EVs) prepared from the human NK cell line NK-92 cultured for 48hrs in serum-free conditions supplemented with 10 ng/ml human recombinant IL-15. The aim was to isolate and define an EV subset with cytolytic activity against tumor cells. Fort his purpose, bulk EVs were separated according to size (via size exclusion chromatography; SEC) or density (density gradient ultracentrifugation; DG-UC).

2022-09-09 | PXD034603 | Pride

Bromodomain and extra-terminal (BET) inhibitors regulate NK cell biology by inhibiting BRD2 mediated NK cytolytic activity and BRD2/BRD4 mediated inflammatory function

Project description:Bromodomain and extra-terminal (BET) inhibitors regulate NK cell biology by inhibiting BRD2 mediated NK cytolytic activity and BRD2/BRD4 mediated inflammatory function

| PRJNA657865 | ENA

Bromodomain and extra-terminal (BET) inhibitors regulate NK cell biology by inhibiting BRD2 mediated NK cytolytic activity and BRD2/BRD4 mediated inflammatory function

Project description:Natural killer cells are innate lymphocytes that play a pivotal role in the immune surveillance and elimination of transformed or virally infected cells. Using a combined chemico-genetic approach, we have identified that BET bromodomains BRD2 and BRD4 are central regulators of NK cell responses. We show that both BRD2 and BRD4 play a key regulatory function in controlling NK cell specific inflammatory responses. However, knockdown of BRD2 but not BRD4 impairs NK cell cytolytic response, highlighting a redundant role for BRD4 in regulating NK cell killing. We further show that the prototypic monovalent BET inhibitor impairs in vitro NK cell mediated killing of cancer target cells, while the bivalent BET bromodomain AZD5153 does not. We ascribe these differences to the preferential affinity of JQ1(+) to BRD2, while AZD5153 has a higher affinity for BRD4. Our work suggests that inhibiting BET bromodomains may be an effective therapeutic strategy for controlling inflammatory function. Given that BRD2 but not BRD4 inhibition can impair NK cell mediated killing, our findings also have clinical significance in light of the ongoing clinical application of BET bromodomains in oncology.

2021-03-16 | GSE156423 | GEO

IL-21 induces antitumor response in NK cells via CEBPD

Project description:NK cells engineered to express IL-21 (IL-21 NK) acquire strong antitumor activity, with the ability to respond to glioblastoma (GBM) rechallenge in vitro and in vivo. IL-21 NK cells have a unique signature of chromatin accessibility, with CCAAT/Enhancer-Binding Protein (C/EBP), especially CEBPD, serving as key transcription factors regulating their memory response.

2024-07-09 | GSE227098 | GEO

High-throughput single-cell RNA sequencing of tumor-infiltrating NK cells

Project description:High-throughput single-cell RNA-seq of tumor-infiltrating NK cells uncovered an NK subset, exhibiting elevated expression of activation markers, cytolytic molecules, chemokines and cytokines when Hif1a was absent in NK cells.

2020-05-21 | GSE123534 | GEO

Cytokine-enhanced cytolytic activity of Exosomes from NK Cells [small RNA seq]

Project description:Cytokine-enhanced cytolytic activity of Exosomes from NK Cells [small RNA seq]

| PRJNA631792 | ENA

Proteomic profiling of subsets of human primary NK cell-derived extracellular vesicles by LC-MS/MS

Project description:In this study we have compared the proteomic profile of subsets of extracellular vesicles (EVs) prepared from primary human NK cells cultured for 48hrs in serum-free conditions supplemented with 10 ng/ml human recombinant IL-12, IL-15, and IL-18. The aim was to isolate and define an EV subset with cytolytic activity against tumor cells. For this purpose, bulk EVs were separated according to density (density gradient ultracentrifugation; DG-UC) to yield 3 distinct subsets.

2022-09-09 | PXD035977 | Pride

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