Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from UKRV-Mel-15a melanoma-derived clones resistant to cytolysis mediated by Melan-A/MART1 (26-35) cytotoxic T lymphocytes (CTL).

ABSTRACT: Efficient processing of target antigens by the ubiquitin-proteasome-system (UPS) is essential for treatment of cancers by T cell therapies. However, immune escape due to impaired expression of IFN-γ-inducible components of the antigen presentation machinery and consequent inefficient processing of HLA-dependent tumor epitopes can be one important reason for failure of such therapies. Here, we show that repeated short-term co-cultures of Melan-A/MART-1 tumor antigen-expressing melanoma cells with Melan-A/MART-1 (26-35)-specific CTL led to the generation of clones resistant to CTL-mediated cell death. To determine which of the UPS components and its associated pathways was responsible for CTL escape; three UKRV-Mel-15a clones were subjected to microarray gene expression analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE75929 | GEO | 2015/12/12

SECONDARY ACCESSION(S): PRJNA305732

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from UKRV-Mel-15a melanoma-derived clones resistant to cytolysis mediated by Melan-A/MART1 (26-35) cytotoxic T lymphocytes (CTL).

Project description:Efficient processing of target antigens by the ubiquitin-proteasome-system (UPS) is essential for treatment of cancers by T cell therapies. However, immune escape due to impaired expression of IFN-Î³-inducible components of the antigen presentation machinery and consequent inefficient processing of HLA-dependent tumor epitopes can be one important reason for failure of such therapies. Here, we show that repeated short-term co-cultures of Melan-A/MART-1 tumor antigen-expressing melanoma cells with Melan-A/MART-1 (26-35)-specific CTL led to the generation of clones resistant to CTL-mediated cell death. To determine which of the UPS components and its associated pathways was responsible for CTL escape; three UKRV-Mel-15a clones were subjected to microarray gene expression analysis. Three UKRV-Mel-15a-derived melanoma clones were isolated following three repeated short-term exposures to Melan-A/MART (26-35) CTL and harvested for RNA extraction and hybridization on Affymetrix microarrays.

2015-12-12 | E-GEOD-75929 | biostudies-arrayexpress

microRNA levels data from Melan-a cells expressing reduced level of Dicer and control Melan-a cells

Project description:To investigate the molecular mechanism of the hypopigmentation observed in Dicer KO mice, Dicer knockdown was realised in vitro in normal C57BL/6 mouse melanocyte Melan-a cells. Transient transfection of Melan-a cells with siRNA directed against Dicer reduced Dicer protein levels to approximately 40% of that of siScr Melan-a cells 24 hours after transfection. We analyzed the miRnome of Melan-a cells 24 and 48 hours after transfection with siDicer or siScr to understand the molecular mechanisms involved in Dicer-dependent melanocyte migration.

2022-03-22 | GSE128754 | GEO

Gene expression data from Melan-a cells expressing reduced level of Dicer and control Melan-a cells [48 hours]

Project description:To investigate the molecular mechanism of the hypopigmentation observed in Dicer KO mice, Dicer knockdown was realised in vitro in normal C57BL/6 mouse melanocyte Melan-a cells. Transient transfection of Melan-a cells with siRNA directed against Dicer reduced Dicer protein levels to approximately 40% of that of siScr Melan-a cells 48 hours after transfection. We analyzed the transcriptome of Melan-a cells 48 hours after transfection with siDicer or siScr to understand the molecular mechanisms involved in Dicer-dependent melanocyte migration.

2022-03-22 | GSE128756 | GEO

Gene expression data from Melan-a cells expressing reduced level of Dicer and control Melan-a cells [24 hours]

Project description:To investigate the molecular mechanism of the hypopigmentation observed in Dicer KO mice, Dicer knockdown was realised in vitro in normal C57BL/6 mouse melanocyte Melan-a cells. Transient transfection of Melan-a cells with siRNA directed against Dicer reduced Dicer protein levels to approximately 40% of that of siScr Melan-a cells 24 hours after transfection. We analyzed the transcriptome of Melan-a cells 24 hours after transfection with siDicer or siScr to understand the molecular mechanisms involved in Dicer-dependent melanocyte migration.

2022-03-22 | GSE128755 | GEO

Transcriptome and gene/transcript expression profiling in melan-a cells

Project description:The melan-a cell line is derived from immortalized mouse melanocytes obtained from Ink4a-ARF-/- mice. RNA-seq was performed to assess the global nature of transcript and gene expression profiles in melan-a cells. These RNA-seq data, along with separate ChIP-seq performed in melan-a cells (GSE38498), were used to correlate gene expression patterns with the presence or absence of transcription factors of interest.

2016-09-18 | GSE87051 | GEO

Melan-a cells expressing reduced level of Dicer and control Melan-a cells

Project description:Melan-a cells expressing reduced level of Dicer and control Melan-a cells

| PRJNA528796 | ENA

Melan-a mouse melanocytes vs. B16 mouse melanoma cells

Project description:Gene expression profile of melan-a mouse melanocytes vs. B16 mouse melanoma cells. Keywords: Cell type comparison

2008-07-31 | GSE11584 | GEO

Melan-a melanocytes and B16 melanoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE11580: Time course RA-treatment of B16 mouse melanoma cells GSE11584: Melan-a mouse melanocytes vs. B16 mouse melanoma cells Keywords: SuperSeries Refer to individual Series

2008-07-31 | E-GEOD-11588 | biostudies-arrayexpress

microRNA levels data from Melan-a cells expressing reduced level of Dicer and control Melan-a cells

Project description:microRNA levels data from Melan-a cells expressing reduced level of Dicer and control Melan-a cells

| PRJNA528797 | ENA

Molecular signature of CD8+ T cell exhaustion in metastases but not in peripheral blood from melanoma patients

Project description:In chronic viral infections such as HIV-1, HBV and HCV, CD8+ T cells may become ”exhausted”, characterized by progressive functional deficiency. Recently, the underlying mechanisms have been characterized by molecular profiling of virus-specific CD8+ T cells. In contrast, only little is known of self/tumor-specific CD8+ T cells from cancer patients, likely because they are much more difficult to assess. For the first time, we determined the molecular profile of human tumor-specific CD8+ T cells, upon sorting of Melan-A/MART-1 specific T cells directly ex vivo from 19 melanoma patients after vaccination with peptide and CpG. For comparison, we sorted protective T cells specific for the two herpes viruses EBV and CMV. In peripheral blood, we found multiple features of functional effector T cells, with only small but nevertheless significant differences between the three T cell populations, resulting in clean clustering according to antigen specificity. In contrast, Melan-A/MART-1 specific T cells obtained from tumor-infiltrated lymph nodes (TILNs) expressed multiple genes associated with T cell exhaustion, compatible with the known functional deficiencies of T cells in melanoma metastases. We show that individual T cells simultaneously expressed multiple inhibitory receptors implied in functional impairment. Together, the data indicate that in circulation, human tumor-specific T cells have the potential to become competent effector cells. In the tumor environment, however, T cells are exhausted and fail to control malignant disease. Our novel resource data identify mechanisms of functional T cell deficiency in melanoma patients, providing a rational basis for the improvement of immune therapy.

2011-11-22 | GSE24536 | 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