Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [TC1A9_DAC]

ABSTRACT: Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNγ. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNγ treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNγ acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.

ORGANISM(S): Mus musculus

PROVIDER: GSE53466 | GEO | 2014/12/08

SECONDARY ACCESSION(S): PRJNA232060

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [TC1A9_IFN]

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNγ. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNγ treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNγ acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.

2014-12-08 | GSE53467 | GEO

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [RVPC3_DAC]

2014-12-08 | GSE53465 | GEO

Epigenetic regulations in the IFNM-NM-3 signalling pathway: IFNM-NM-3-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [TC1A9_IFN]

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNM-NM-3. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNM-NM-3 treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNM-NM-3 acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity. TC-1/A9 cultured cells treated with IFN gama or nothing. 3 biological replicates per condition.

2014-12-08 | E-GEOD-53467 | biostudies-arrayexpress

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNM-NM-3. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNM-NM-3 treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNM-NM-3 acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity. TC-1/A9 cultured cells treated with DAC/TSA or nothing. 3 biological replicates per condition.

2014-12-08 | E-GEOD-53466 | biostudies-arrayexpress

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNM-NM-3. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNM-NM-3 treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNM-NM-3 acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity. RVP3 cultured cells treated with DAC/TSA or nothing. 3 biological replicates per condition.

2014-12-08 | E-GEOD-53465 | biostudies-arrayexpress

IFNγ treatment restores TAP-dependent presentation competence of PD-L1 sensitive PDAC cells

Project description:For immunotherapy, there is an urgent need to restore presentation-competence of cancer cells with defects in MHC-I processing/presentation. We identified two tumor-specific antigens expressed in the ER of pancreatic ductal adenocarcinoma cells (PDACCs) that induced effector CD8 T cells either independent (Cripto-1-Kb/Cr16-24) or dependent (gp70-Kb/p15E) on TAP-mediated antigen processing/presentation by DNA immunization. In systematic analyses, we showed that transplantation into syngeneic C57BL/6J mice or IFNγ-treatment in vitro upregulated MHC-I but also co-inhibitory PD-L1 molecules on PDACCs. IFNγ-treated PDACCs efficiently formed solid tumors in transplanted C57BL/6J and PD-L1-/- but were rejected in PD-1-/- mice. PDACCs induced a prophylactic immunity against tumor transplants in C57BL/6J mice when irradiated at day 2-3 post IFNγ-treatment, thereby silencing the tumor-initiated immune-suppressive PD-L1/PD-1-signaling axis. Immune-protection correlated with a significant enhanced induction of CD8 T cells against the TAP- but not the TAP-dependent antigen/epitope.

2020-08-06 | GSE140397 | GEO

Project description:Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes

| PRJNA232057 | ENA

Mus musculus

| PRJNA232059 | ENA

Mus musculus

| PRJNA232060 | ENA

Mus musculus

| PRJNA232058 | ENA