Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [scRNA-seq]

ABSTRACT: STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [scRNA-seq]

PROVIDER: PRJNA974914 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia.

Project description:STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia.

| PRJNA974904 | ENA

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RRBS]

Project description:STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RRBS]

| PRJNA974913 | ENA

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RNASEQ_AML_CPGDOX]

Project description:STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RNASEQ_AML_CPGDOX]

| PRJNA974911 | ENA

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RNASEQ_AML_DECSCR]

Project description:STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RNASEQ_AML_DECSCR]

| PRJNA974912 | ENA

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RNASEQ_AML_CPGDOX]

Project description:Cultured acute myeloid leukemia (AML) blasts can differentiate into antigen-presenting cells but achieving leukemic cell immunogenicity proved challenging in clinical setting. Despite expressing multiple immunostimulatory receptors, such as Toll-like Receptor 9 (TLR9), AML cells resist immunostimulation. We previously demonstrated that eliminating Signal Transducer and Activator of Transcription 1 and 3 (STAT1/3) signaling in AML cells using decoy DNA strategy (CpG-STAT3dODN) synergized with TLR9 stimulation and resulted in T cell-mediated leukemia regression. Here, we interrogated the molecular underpinnings of CpG-STAT3dODN-driven differentiation and immunogenicity of mouse Cbfb/MYH11/Mpl AML. The transcriptional profiling of AML cells isolated from mice after inducible Stat3 silencing plus TLR9 stimulation or CpG-STAT3dODN treatment, revealed comparable upregulation of genes related to myeloid cell differentiation (Irf8, Cebpa) and immune stimulation (Gadd45a, Ciita, Il12a, Ifng) but decreased expression of leukemia-promoting Runx1 and Run1t1. The conditional Irf8 silencing in AML cells almost completely abrogated TLR9-driven leukemia cell differentiation. The AML cell reprogramming by CpG-STAT3dODN was likely regulated epigenetically as revealed by reduced global promoter hypomethylation of crucial myeloid cell differentiation and immune activation genes. These changes were associated with reduced expression of known STAT3 targets, DNMT1 and DNMT3a/b. Finally, we provide initial evidence of anti-leukemic effects of CpG-STAT3 inhibitor against human AML model in humanized mice. Our studies suggest that, beyond oncogenic functions, STAT3 in AML cells may be a primary checkpoint in control of immune-stimulatory and differentiation driving effects. These findings support further development of CpG-STAT3 inhibitors as a new bi-functional agents for AML immunotherapy.

2024-07-23 | GSE233095 | GEO

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RRBS]

2024-07-23 | GSE233097 | GEO

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [RNASEQ_AML_DECSCR]

2024-07-23 | GSE233096 | GEO

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia [scRNA-seq]

2024-07-23 | GSE233098 | GEO

STAT3 inhibition permits epigenetic reprogramming and TLR9/IRF8-driven differentiation of inv(16) acute myeloid leukemia.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-23 | GSE233099 | GEO

IRF8 REGULATES EXPRESSION OF ANTIGEN PROCESSING AND PRESENTATION PATHWAYS IN MYELOID CELLS

Project description:In this study, we have used transcript profiling with microarrays in bone marrow-derived macrophages (BMDMs) to systematically identify genes transcriptionally regulated by IRF8 during ontogeny and maturation of macrophages, and in response of these cells to combined exposure to IFNgamma and Tlr9 ligand (CpG). For this, we used an experimental strategy based on the co-segregation of IRF8-dependent differential gene expression in macrophages from [BALB/c X BXH2] F2 animals selected for homozygosity for either wild type (wt; IRF8R294) or mutant (IRF8C294) IRF8 alleles. The study of IRF8-associated gene expression differences in individual animals of mixed genetic background, allows one to distinguish true IRF8-dependent effects on gene expression from unrelated differences in gene expression associated with intrinsic differences in genetic background but unrelated to IRF8.

2011-04-27 | E-MEXP-2962 | biostudies-arrayexpress

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