Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibition of Tumor Growth and Metastasis by EMMPRIN Multiple Antigenic Peptide (MAP) Vaccination Is Mediated by Immune Modulation

ABSTRACT: We report here that a EMMPRINs-specific cancer peptide vaccination, where the peptide was modified and synthesied as a multiple antigenic peptide (MAP), significantly inhibited tumor growth and metastases. Specifically, we describe changes in the gene expression profile as assessed by RNAseq in tumors derived from mice implanted with the colon tumorigenic carcinoma (CT26 cells), and vaccinated with either a control scrambled multiple antigenic peptide (Scr-MAP) or with an epitope-specific EMMPRIN multiple antigenic peptide (designated 161-MAP).

ORGANISM(S): Mus musculus

PROVIDER: GSE85440 | GEO | 2019/08/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

TCR variable regions transcripts of CT26-shppp2r1a and CT26-scr samples

Project description:TCR variable regions transcripts of three CT26-shppp2r1a samples and three CT26-scr samples

2021-11-20 | GSE189092 | GEO

Response of peripheral blood mononuclear cells from patients with allergy to cat and silver birch wood derived antigenic peptide stimulation.

Project description:CD4 T cell responses are characterized based on a limited number of molecular markers selected from exisiting knowledge. The goal of the experiment was to assess antigenic-peptide specific T-cell responses in vitro without bias using microarrays. PBMCs were isolated from 2 donors with allergy. The cells were stimulated with antigenic peptides derived from silver birch wood and cat for 24 hours. Unstimulated cells were cultured without the peptides for 24 hours.

2016-08-15 | E-GEOD-72373 | biostudies-arrayexpress

Response of peripheral blood mononuclear cells from patients with allergy to cat and silver birch wood derived antigenic peptide stimulation.

2016-08-15 | GSE72373 | GEO

RNA sequencing data of CT26-shppp2r1a and CT26-scr samples

Project description:RNA sequencing data of CT26-shppp2r1a and CT26-scr samples

| PRJNA756949 | ENA

TCR variable regions transcripts of CT26-shppp2r1a and CT26-scr samples

Project description:TCR variable regions transcripts of CT26-shppp2r1a and CT26-scr samples

| PRJNA781570 | ENA

antigenic KPC model_bulk pancreas RNASeq

Project description:antigenic KPC model_bulk pancreas RNASeq

| PRJNA544120 | ENA

RNA sequencing data of CT26-shppp2r1a and CT26-scr samples

Project description:Goal: Microsatellite-instable (MSI) tumors are one of the few cancers that respond to immune checkpoint blockade (ICB); however, the mechanism of MSI status development is unclear. Here, we report that protein phosphatase 2A (PP2A) deletion or inactivation converted cold microsatellite-stable (MSS) into MSI tumors. Objectives: Using RNA sequencing data of three CT26-shppp2r1a data and a CT26-scr data, we demonstrate that these intestinal tumors display differential core driver pathways.

2021-08-26 | GSE182571 | GEO

Mus musculus

Project description:Inhibition of Tumor Growth and Metastasis by EMMPRIN Multiple Antigenic Peptide (MAP) Vaccination Is Mediated by Immune Modulation

| PRJNA338459 | ENA

Gene expression of murine repeatedly activated Th1 cells after miR-31 knock down

Project description:Gene expression of murine repeatedly activated Th1 cells 36h, 48h and 72h after miR-31 inhibition using a specific antagomir (Antagomir-31) compared to a scrambled controll (Antagomir-SCR).

2018-12-19 | GSE122223 | GEO

Targeting the SIN3A-PF1 Interaction inhibits Epithelial to Mesenchymal Transition and Maintenance of a Stem Cell Phenotype in Triple Negative Breast Cancer (Expression)

Project description:Triple negative breast cancer (TNBC) is characterized by a poorly differentiated phenotype and limited treatment options. Aberrant epigenetics in this subtype represent a potential therapeutic opportunity, but a better understanding of the mechanisms contributing to the TNBC pathogenesis is required. The SIN3 molecular scaffold performs a critical role in multiple cellular processes, including epigenetic regulation, and has been identified as a potential therapeutic target. Using a competitive peptide corresponding to the SIN3 interaction domain of MAD (Tat-SID), we investigated the functional consequences of selectively blocking the paired amphipathic helix (PAH2) domain of SIN3. Here, we report the identification of the SID-containing adaptor PF1 as a factor required for maintenance of the TNBC stem cell phenotype and epithelial to mesenchymal transition (EMT). Tat-SID peptide blocked the interaction between SIN3A and PF1, leading to epigenetic modulation and transcriptional downregulation of TNBC stem cell and EMT markers. Importantly, Tat-SID treatment led to a reduction in primary tumor growth and disseminated metastatic disease in vivo. In support of these findings, knockdown of PF1 expression phenocopied treatment with Tat-SID both in vitro and in vivo. These results demonstrate a critical role for a complex containing SIN3A and PF1 in TNBC and provide a rational for its therapeutic targeting. Sub-confluent cultures of MDA-MB-231 cells were treated with 1ÂµM Tat-SID peptide or 1ÂµM Tat-Scr scrambled control peptide for 24hr.

2015-11-02 | E-GEOD-73278 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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