Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PTIR1 acts as a suppressor of immunoproteasome and promotes cancer immune resistance [TILs 10x scRNA-seq]

ABSTRACT: Cancer cells evade host immune surveillance by virtue of poor immunogenicity. We identify a novel oncogene that acts as a promotor of tumor immune resistance, designated as PTIR1. Tumor-intrinsic PTIR1 is induced by RNA splicing and highly correlated with poor outcome of patients with cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE200190 | GEO | 2025/04/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

PTIR1 acts as a suppressor of immunoproteasome and promotes cancer immune resistance

Project description:Cancer cells evade host immune surveillance by virtue of poor immunogenicity. We identify a novel oncogene that acts as a promotor of tumor immune resistance, designated as PTIR1. Tumor-intrinsic PTIR1 is induced by RNA splicing and highly correlated with poor outcome of patients with cancer.

2024-02-19 | GSE168862 | GEO

PTIR1 acts as a suppressor of immunoproteasome and promotes cancer immune resistance [TILs 10x scRNA-seq]

Project description:PTIR1 acts as a suppressor of immunoproteasome and promotes cancer immune resistance [TILs 10x scRNA-seq]

| PRJNA823649 | ENA

Mechanisms of immunoediting and immune evasion in AML1-ETO (AE) NrasG12D AML.

Project description:Immunoediting describes the dynamic sculpting of cancer cells to evade cancer immune control, thereby enabling the development of tumors in an immunocompetent host resulting in the outgrowth of cancer cells with reduced immunogenicity.

2023-02-23 | GSE164951 | GEO

Mechanisms of immunoediting and immune evasion in MLL-AF9 AML.

2023-02-23 | GSE207316 | GEO

Pancreatic cancer-derived exosomes induce apoptosis of T lymphocytes through the p38 MAPK signal transduction pathway

Project description:Pancreatic cancer is the fourth most lethal malignancy, which is characterized by poor immunogenicity. Pancreatic cancer cells take various strategies to suppress host immune response, evade immune defenses, and facilitate tumor growth and development. As a mode of long-range intercellular communication, cancer-derived exosomes contribute to the impairment of the immune system. However, the mechanisms that induce changes in the activities of signal transduction pathways in immune cells, which are influenced by tumor-derived exosomes, are poorly understood. We treated peripheral T lymphocytes with pancreatic cancer-derived exosomes, performed RNA-seq and Gene Set Enrichment Analysis to explore the pivotal signaling pathway that mediates apoptosis in exosomes-treated T lymphocytes.

2018-06-18 | GSE115831 | GEO

Rational engineering of minimally immunogenic nucleases for gene therapy

Project description:Genome editing using CRISPR-Cas systems is a promising avenue for the treatment of genetic diseases. However, cellular and humoral immunogenicity of genome editing tools, which originate from bacteria, complicates their clinical use. Here we report reduced immunogenicity (Red)(i)-variants of two clinically-relevant nucleases, SaCas9 and AsCas12a. Through MHC-associated peptide proteomics (MAPPs) analysis, we identified putative immunogenic epitopes on each nuclease. Then, we used computational modeling to rationally design these proteins to evade the immune response. SaCas9 and AsCas12a Redi variants were substantially less recognized by adaptive immune components, including reduced binding affinity to MHC molecules and attenuated generation of cytotoxic T cell responses, while maintaining wild-type levels of activity and specificity. In vivo editing of PCSK9 with SaCas9.Redi.1 was comparable in efficiency to wild-type SaCas9, but significantly reduced undesired immune responses. This demonstrates the utility of this approach in engineering proteins to evade immune detection.

2024-11-07 | PXD054579 | Pride

Project description:Designated breeding

| PRJNA1134419 | ENA

CD8+ TILs in NSCLC differentiate into TEMRA via a bifurcated trajectory, deciphering immunogenicity of tumor-antigens

Project description:CD8+ tumor-infiltrating lymphocytes (TILs) comprise phenotypically and functionally heterogeneous subpopulations. Of these, effector memory CD45RA-expressing CD8+ T cells (Temra) have been discovered and characterized as the most terminally differentiated subset. However, their exact ontogeny and physiological importance in association with tumor progression remain poorly understood. We analyzed primary tumors and peripheral blood samples from 26 patients with non-small cell lung cancer and analyzed their phenotypes and functional characteristics using flow cytometry, RNA-sequencing, and bioinformatics. We found that tumor-infiltrating Temra (tilTemra) cells largely differ from peripheral blood Temra (pTemra), with distinct transcriptomes and functional properties. Notably, although majority of the pTemra was CD27-CD28- double-negative (DN), a large fraction of tilTemra population was CD27+CD28+ double-positive (DP), a characteristic of early-stage, less differentiated effector cells. Trajectory analysis revealed that CD8+ TILs undergo a divergent sequence of events for differentiation into either DP or DN tilTemra. Such a differentiation toward DP tilTemra relied on persistent expression of CD27 and CD28 and was associated with weak T cell receptor engagement. Thus, a higher proportion of DP Temra was correlated with lower immunogenicity of tumor antigens and consequently lower accumulation of CD8+ TILs. These data suggest a complex interplay between CD8+ T cells and tumors and define DP Temra as a unique subset of tumor-specific CD8+ TILs that are produced in patients with relatively low immunogenic cancer types, predicting immunogenicity of tumor antigens and CD8+ TIL counts, a reliable biomarker for successful cancer immunotherapy.

2021-09-14 | GSE184053 | GEO

Direct Comparative Analyses of 10X Genomics Chromium and Smart-seq2.

Project description:Single-cell RNA sequencing (scRNA-seq) is generally used for profiling transcriptome of individual cells. The droplet-based 10X Genomics Chromium (10X) approach and the plate-based Smart-seq2 full-length method are two frequently used scRNA-seq platforms, yet there are only a few thorough and systematic comparisons of their advantages and limitations. Here, by directly comparing the scRNA-seq data generated by these two platforms from the same samples of CD45- cells, we systematically evaluated their features using a wide spectrum of analyses. Smart-seq2 detected more genes in a cell, especially low abundance transcripts as well as alternatively spliced transcripts, but captured higher proportion of mitochondrial genes. The composite of Smart-seq2 data also resembled bulk RNA-seq data more. For 10X-based data, we observed higher noise for mRNAs with low expression levels. Approximately 10%-30% of all detected transcripts by both platforms were from non-coding genes, with long non-coding RNAs (lncRNAs) accounting for a higher proportion in 10X. 10X-based data displayed more severe dropout problem, especially for genes with lower expression levels. However, 10X-data can detect rare cell types given its ability to cover a large number of cells. In addition, each platform detected distinct groups of differentially expressed genes between cell clusters, indicating the different characteristics of these technologies. Our study promotes better understanding of these two platforms and offers the basis for an informed choice of these widely used technologies.

| S-EPMC8602399 | biostudies-literature

Global gene expression profile of CD8+ TILs from WT and B7S1 KO mice

Project description:B7S1 negatively regulates T cells and its expression correlates with poor prognosis of cancer patients. In order to understand how B7S1 signaling contributes to dysfunction of CD8+ T cell in the TME, we conducted transcriptional analysis of OVA-specific CD8+ TILs and different TIL subsets from E.G7-bearing WT and B7S1 KO mice (Day 21).

2018-04-03 | GSE110249 | 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