Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

ABSTRACT: Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

PROVIDER: PRJNA1205401 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31867057_1.fastq.gz	Fastqsanger.gz
	SRR31867057_2.fastq.gz	Fastqsanger.gz
	SRR31867058_1.fastq.gz	Fastqsanger.gz
	SRR31867058_2.fastq.gz	Fastqsanger.gz
	SRR31867059_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

Project description:Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

| PRJNA1098589 | ENA

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

Project description:Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

| PRJNA1098587 | ENA

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

Project description:Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

| PRJNA1098591 | ENA

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

Project description:Melanoma is one of the tumor types with the highest risk of brain metastasis. However, the biology of melanoma brain metastasis and the contribution of the brain immune microenvironment to the responses to therapies remain insufficiently characterized. By using preclinical models and single-cell transcriptomics, we identify a mechanism to promote antitumor immunity in melanoma brain metastasis. We show that activation of the Rela/NF-kB pathway in microglia promotes melanoma brain metastasis and that targeting this pathway elicits microglia reprogramming towards a proinflammatory phenotype that enhances antitumor immunity and reduces brain metastatic burden. Additionally, proinflammatory microglial markers in melanoma brain metastasis correlate with better responses to immune checkpoint inhibitors in patients and we show that Rela/NF-kB targeting improves responses to these therapies in the brain. Thus, we propose targeting Rela/NF-kB in activated microglia as a strategy to promote antitumor immunity and responses to immune checkpoint inhibitors in melanoma brain metastasis.

2025-02-07 | GSE285670 | GEO

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

Project description:Melanoma is one of the solid tumor types with the highest risk of brain metastasis. However, the biology of melanoma brain metastasis and the contribution of the brain immune microenvironment to the responses to therapies remain insufficiently characterized. By using preclinical models and single-cell transcriptomics, we identify microglia, as critical regulators of melanoma biology in the brain. We show that activation of the Rela/NF-kB pathway in microglia promotes melanoma brain metastasis and that targeting this pathway elicits microglia reprogramming towards a pro-inflammatory phenotype that enhances anti-tumor immunity and reduces brain metastatic burden. Additionally, canonical and pro-inflammatory microglial markers in melanoma brain metastasis correlate with better responses to immune checkpoint inhibitors in patients and we show that Rela/NF-kB targeting improves responses to these therapies in the brain. Thus, we propose targeting Rela/NF-kB in activated microglia as a strategy to promote anti-tumor immunity and to improve the response to immune checkpoint inhibitors in melanoma brain metastasis.

2025-02-07 | GSE263622 | GEO

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

2025-02-06 | GSE263625 | GEO

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

2025-02-07 | GSE263623 | GEO

Inhibition of MBTPS1 enhances antitumor immunity and potentiates anti-PD-1 immunotherapy

Project description:In this project, we transfected MC38 cells with Flag-tagged Mbtps1 or vector control. After that, we performed immunoprecipitation–mass spectrometry analysis to search the interacting proteins of MBTPS1. In our study, We observed that the loss of membrane-bound transcription factor site-1 protease (MBTPS1) in tumor cells enhanced antitumor immunity and potentiated anti-PD-1 therapy. Mechanistic studies revealed that tumor cell-intrinsic MBTPS1 competed with USP13 for binding to STAT1, thereby disrupting USP13-dependent deubiquitination and stabilization of STAT1. MBTPS1 deficiency induced CXCR3+ CD8+ T cell infiltration by upregulating STAT1-transcribed chemokines including CXCL9, CXCL10 and CXCL11. Notably, the regulatory role of MBTPS1 in antitumor immunity operates independently of its classic function in cleaving membrane-bound transcription factors. Collectively, our results provide a theoretical basis for MBTPS1 as a potential immunotherapy target and also as a predictor of immunotherapy efficacy.

2025-04-11 | PXD053978 | Pride

Exercise-induced microbiota metabolite enhances CD8 T cell antitumor immunity promoting immunotherapy efficacy

Project description:Exercise-induced microbiota metabolite enhances CD8 T cell antitumor immunity promoting immunotherapy efficacy

| PRJNA1248760 | ENA

Exercise-induced microbiota metabolite enhances CD8 T cell antitumor immunity promoting immunotherapy efficacy

Project description:Exercise improves immune checkpoint inhibitor (ICI) efficacy in cancers like melanoma, however, the mechanisms through which exercise mediates this antitumor effect remain obscure. Here we identify the gut microbiota as playing a previously unrecognized, critical role in how exercise improves ICI efficacy in preclinical melanoma. Our study demonstrates that exercise stimulates microbial one-carbon metabolism, increasing levels of the metabolite formate, which subsequently enhances Tc1-mediated ICI efficacy. We further establish that microbiota-derived formate is both sufficient and required to enhance Tc1 cell fate in vitro and promote tumor antigen-specific Tc1 immunity in vivo. Mechanistically, we identified the transcription factor nuclear factor erythroid 2-related factor-2 (Nrf2) as a crucial mediator of formate-driven Tc1 function enhancement in vitro and a key player in the exercise-mediated antitumor effect in vivo. Finally, we identify human microbiota-derived formate as a potential biomarker of enhanced Tc1-mediated antitumor immunity and support its functional role in driving melanoma suppression.

2025-07-23 | GSE294230 | 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