Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

ABSTRACT: Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

PROVIDER: PRJNA874419 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21278558.fastq.gz	Fastqsanger.gz
	SRR21278559.fastq.gz	Fastqsanger.gz
	SRR21278560.fastq.gz	Fastqsanger.gz
	SRR21278561.fastq.gz	Fastqsanger.gz
	SRR21278562.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

Project description:Methyltransferase-like 3 (METTL3), a core catalytic subunit for RNA N6-methyladenosine (m6A) modification, plays a crucial role in regulating gene expression to govern various physiological and pathological processes. However, whether and how METTL3 regulates TME and anti-tumor immunity in non-small-cell lung cancer (NSCLC) remains poorly understood. To understand the function and mechanism of METTL3 in NSCLC TME, we compare the differential expression genes (DEGs) in STM2457 (METTL3 specific inhibitor) versus DMSO treated lewis lung carcinoma cells (LLC).

2023-01-31 | GSE212177 | GEO

Blocking of CA-MSC-induced desmoplasia reprograms the tumor immune microenvironment and enhances cancer immunotherapy

Project description:Blocking of CA-MSC-induced desmoplasia reprograms the tumor immune microenvironment and enhances cancer immunotherapy

| PRJNA767377 | ENA

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Human_Mulitome_Cohort1]

Project description:Mycobacterium bovis Bacillus Calmette-Guérin (BCG) is the vaccine against tuberculosis and an immunotherapy for bladder cancer. When administered intravenously, BCG reprograms bone marrow hematopoietic stem and progenitor cells (HSPCs), leading to heterologous protection against infections. Whether HSPC reprogramming contributes to the anti-tumor effects of BCG administered into the bladder is unknown. We demonstrate that BCG administered in the bladder colonizes the bone marrow and, in both mice and humans, reprograms HSPCs to alter and amplify myelopoiesis. BCG-reprogrammed HSPCs are sufficient to confer augmented anti-tumor immunity through production of neutrophils, monocytes, and dendritic cells that broadly remodel the tumor microenvironment, drive T cell-dependent anti-tumor responses, and synergize with checkpoint blockade. We conclude that bladder BCG acts systemically through hematopoiesis, highlighting the broad potential of HSPC reprogramming to enhance the innate drivers of T cell-dependent tumor immunity.

2025-04-22 | GSE295277 | GEO

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Human_Multiome_Cohort2

2025-04-22 | GSE295308 | GEO

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Mouse_Multiome]

2025-04-22 | GSE295006 | GEO

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Mouse_LSK_ATAC]

2025-04-22 | GSE295004 | GEO

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Mouse_CD45_scRNA]

2025-04-22 | GSE295003 | GEO

Chemohormonal Therapy Remodels Prostate Cancer Immune Microenvironment and Enhances Checkpoint Inhibitor-based immunotherapy

Project description:Checkpoint blockade immunotherapy is a promising strategy in cancer treatment, depending on a favorable preexisting tumor immune microenvironment. However, prostate cancer is usually considered as an immune “cold” tumor with the poor immunogenic response and low density of tumor-infiltrating immune cells. This research uses samples from prostate cancer patients showing that docetaxel-based chemohormonal therapy reprograms the immune microenvironment and increases tumor-infiltrating T cells. Mechanistically, docetaxel treatment activates the cGAS/STING pathway and induces the type I interferon signaling, which may boost T cell-mediated immune response. In a murine prostate cancer model, chemohormonal therapy sensitizes tumor-bearing mice to PD1-blockade therapy. These findings demonstrate that docetaxel-based chemohormonal therapy activates prostate cancer immunogenicity and acts cooperatively with anti-PD-1 checkpoint blockade, providing a combination immunotherapy strategy that would lead to better therapeutic benefit for prostate cancer.

2022-08-01 | GSE193898 | GEO

METTL3 promotes translation in human cancer cells

Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells

2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress

Tumor microenvironment remodeling after neoadjuvant immunotherapy in non-small cell lung cancer revealed by single-cell RNA sequencing

Project description:To address the potential therapy-resistant mechanisms and underly the changes of tumor microenvironment (TME) after immunotherapy, we performed scRNA-seq and bulk RNA-seq from the patients with resectable non-small cell lung cancer (NSCLC) before and after PD-1 blockade combined with chemotherapy. We found that the combined therapy significantly remodeled the immune cell compartments in the TME. Patients with different pathologic responses had distinct characteristics of malignant cells and immune cell compositions. Our study provided several potential biomarkers for future immunotherapy and novel strategies to improve response.

2023-03-21 | GSE207422 | 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