Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [RNA-seq]

ABSTRACT: Despite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of tumor progression. Functional studies showed that loss of DMAP1 exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, loss of DMAP1 causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating tumor-intrinsic immune signaling and enhancing anti-tumor immune response during cancer cell growth. Clinical data analyses revealed that high DMAP1 expression is associated with reduced immune infiltration, a “cold” tumor microenvironment, and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1's function in lung cancer development and offer a scientific basis for designing novel treatment approaches.

ORGANISM(S): Mus musculus

PROVIDER: GSE304428 | GEO | 2026/06/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [CUT&Tag]

Project description:Despite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of tumor progression. Functional studies showed that loss of DMAP1 exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, loss of DMAP1 causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating tumor-intrinsic immune signaling and enhancing anti-tumor immune response during cancer cell growth. Clinical data analyses revealed that high DMAP1 expression is associated with reduced immune infiltration, a “cold” tumor microenvironment, and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1's function in lung cancer development and offer a scientific basis for designing novel treatment approaches.

2026-06-24 | GSE304430 | GEO

DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [scRNA-seq]

2026-06-24 | GSE304429 | GEO

DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [RNA-seq]

Project description:DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [RNA-seq]

| PRJNA1301296 | ENA

DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [CUT&Tag]

Project description:DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [CUT&Tag]

| PRJNA1301297 | ENA

DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [scRNA-seq]

Project description:DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [scRNA-seq]

| PRJNA1301299 | ENA

Wilson2012 - tumor vaccine efficacy

Project description:The paper describes a model of antitumor vaccine therapy. Created by COPASI 4.25 (Build 207) This model is described in the article: A Mathematical Model of the Enhancement of Tumor Vaccine Efficacy by Immunotherapy Shelby Wilson and Doron Levy Bull Math Biol. 2012 July ; 74(7) Abstract: TGF-β is an immunoregulatory protein that contributes to inadequate antitumor immune responses in cancer patients. Recent experimental data suggests that TGF-β inhibition alone, provides few clinical benefits, yet it can significantly amplify the anti-tumor immune response when combined with a tumor vaccine. We develop a mathematical model in order to gain insight into the cooperative interaction between anti-TGF-β and vaccine treatments. The mathematical model follows the dynamics of the tumor size, TGF-β concentration, activated cytotoxic effector cells, and regulatory T cells. Using numerical simulations and stability analysis, we study the following scenarios: a control case of no treatment, anti-TGF-β treatment, vaccine treatment, and combined anti-TGF-β vaccine treatments. We show that our model is capable of capturing the observed experimental results, and hence can be potentially used in designing future experiments involving this approach to immunotherapy. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

2024-09-02 | BIOMD0000000791 | BioModels

Super-paramagnetic iron oxide nanoparticles reprogram the tumor microenvironment and reduce lung cancer growth

Project description:Tumor associated macrophages (TAMs) are known to play a role in a multitude of processes that facilitate lung cancer growth, including the suppression of tumoricidal immune activation and the absorption of chemotherapeutics. Therefore, deciphering new therapies to reprogram TAMs towards an anti-tumor phenotype is at the cutting-edge of therapy development. The presence of iron-loaded macrophages has been associated with a better prognosis in lung cancer patients. Iron accumulation in macrophages stimulates pro-tumoricidal macrophage activity that triggers cytotoxic T-cell responses in the tumor microenvironment. In this study, we propose super-paramagnetic iron oxide nanoparticles (SPIONs) as a promising anti-lung cancer adjuvant therapy to reduce tumor cell growth. We used SPIONs to target iron to macrophages and observed that SPION-loaded macrophages reduced tumor cell growth due to the oxidative stress. Additionally, we found that SPIONs completely rewire the tumor microenvironment in mice towards an anti-tumor state and that in combination with crizotinib, a lung cancer targeted therapy, SPIONs show an additive effect in decelerating tumor growth

2024-04-18 | PXD040145 | Pride

RNA-seq of two Pancreatic ductal adenocarcinoma (PDAC) cell lines BxPC-3 and PANC-1 treated with 3x8 Gy X-rays without or with the PARP7 inhibitors RBN-2397 and KMR-206

Project description:Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer and is associated with a dismal prognosis. Due to late diagnosis, the disease is frequently locally advanced and not amenable to surgical resection, and only a small fraction of patients benefit from radio- or chemotherapy. Immunotherapy has shown limited efficacy as monotherapy, largely due to the profoundly immunosuppressive tumor microenvironment. Recent studies have demonstrated that anti-tumor immune responses can be elicited in pancreatic cancer through activation of the cGAS-STING and RIG-I-MAVS pathways, particularly in the context of radiation therapy. Notably, a hypofractionated radiation regimen of 3×8 Gy has been shown to be more effective than a single dose in inducing immunogenic cell death, type I interferon (IFN-I) signaling, and pro-inflammatory cytokine production. PARP7 inhibitors have also been reported to promote anti-tumor immunity by activating IFN-I responses in lung and colon cancer. Here, we show that in PDAC cells, PARP7 inhibition potentiates the effects of radiation by enhancing STING- and NF-κB dependent immunogenic signaling, inflammatory gene expression, pro-inflammatory cytokine release, immunogenic cell death, and immune cell activation. We performed RNA-seq analysis of all two PDAC cell lines treated with 3x8 Gy alone, or in combination with two different PARP7 inhibitors RBN-2397 and KMR-206.

2026-06-01 | E-MTAB-16549 | biostudies-arrayexpress

circNDUFB2 inhibits non-small cell lung cancer progression via destabilizing IGF2BPs and activating anti-tumor immunity

Project description:circNDUFB2 inhibits non-small cell lung cancer progression via destabilizing IGF2BPs and activating anti-tumor immunity

| PRJNA658508 | ENA

Rhodes2019 - Immune-Mediated theory of Metastasis

Project description:Abstract: Accumulating experimental and clinical evidence suggest that the immune response to cancer is not exclusively anti-tumor. Indeed, the pro-tumor roles of the immune system - as suppliers of growth and pro-angiogenic factors or defenses against cytotoxic immune attacks, for example - have been long appreciated, but relatively few theoretical works have considered their effects. Inspired by the recently proposed "immune-mediated" theory of metastasis, we develop a mathematical model for tumor-immune interactions at two anatomically distant sites, which includes both anti- and pro-tumor immune effects, and the experimentally observed tumor-induced phenotypic plasticity of immune cells (tumor "education" of the immune cells). Upon confrontation of our model to experimental data, we use it to evaluate the implications of the immune-mediated theory of metastasis. We find that tumor education of immune cells may explain the relatively poor performance of immunotherapies, and that many metastatic phenomena, including metastatic blow-up, dormancy, and metastasis to sites of injury, can be explained by the immune-mediated theory of metastasis. Our results suggest that further work is warranted to fully elucidate the pro-tumor effects of the immune system in metastatic cancer.

2024-09-02 | BIOMD0000000926 | BioModels

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