Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

ABSTRACT: Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

PROVIDER: PRJNA831273 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

Project description:How to identify subgroups of PCa patients for immune checkpoint therapy (ICT) remains not fully understood. Basic helix-loop-helix family member e22 (Bhlhe22) is upregulated in bone metastatic PCa and drives an immunosuppressive bone TME. Tumoral Bhlhe22 mediates the high expression of colony stimulating factor 2 (CSF2), which results in the infiltration of myeloid-derived suppressor cells (MDSCs) and prolonged immunocompromised T cell status. Here, we reveal the immunosuppressive mechanism of tumoral Bhlhe22 and provide a prospective ICT combination therapeutic for Bhlhe22+ PCa patients.

2022-11-18 | GSE201381 | GEO

Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

2022-11-18 | GSE206108 | GEO

Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

Project description:Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

| PRJNA849217 | ENA

Label free quantitativeproteomics of MDSCs

Project description:We sorted the MDSCs from the bone marrows of B16-F10 tumor-bearing mice and the naive mice. In addition, we cultured MDSCs in vitro to determine the effect of DOX (5µM).

2022-02-17 | PXD027863 | Pride

Genome-wide sequencing of cultured MDSCs obtained from bone marrow of lnc57Rik ko , lncGM1082 ko and WT mice.

Project description:To fully elucidate the effects of long non-coding RNA 5730403I07Rik (lnc57Rik) and lncGM1082 on myeloid-derived suppressor cell (MDSCs), we generated lnc57Rik knockout (KO) and lncGM1082 ko mice. Then bone marrow cells were obtained from the femurs of C57BL/6, lnc57Rik KO, or lncGM1082 ko mice and cultured in RPMI-1640 medium supplemented with GM-CSF plus IL6 for 4 days. We further performed a high-throughput sequencing analysis in cultured MDSCs obtained from bone marrow of lnc57Rik ko, lncGM1082 ko and wild type (WT) mice.

2022-03-03 | GSE197566 | GEO

Mouse Myeloid panel on G-MDSCs from treated tumors

Project description:Immune checkpoint inhibition (ICI) has revolutionized treatment in cancers that are naturally immunogenic by enabling infiltration of T cells into the tumor microenvironment (TME) and promoting cytotoxic signaling pathways. Tumors possessing complex immunosuppressive TME’s such as breast and pancreatic cancers present unique therapeutic obstacles as response rates to ICI remain low. Such tumors often recruit myeloid-derived suppressor cells (MDSCs) whose functioning prohibits both T-cell activation and infiltration. We attempted to sensitize these tumors to ICI using epigenetic modulation to target MDSC trafficking and function to foster a less immunosuppressive TME. We showed that combining a histone deacetylase inhibitor, entinostat (ENT), with anti–PD-1, anti–CTLA-4, [A1] [A2] or both, significantly improved tumor-free survival in both the HER2/neu transgenic breast cancer and the Panc02 metastatic pancreatic cancer mouse models. Using flow cytometry, gene expression profiling, and ex vivo functional assays, we characterized populations of tumor-infiltrating lymphocytes (TILs) and MDSCs, as well as their functional capabilities. We showed that addition of ENT to checkpoint inhibition led to significantly decreased suppression by granulocytic-MDSCs in the TME of both tumor types. We also demonstrated an increase in activated granzyme-B–producing CD8+ T effector cells in mice treated with combination therapy. Gene expression profiling of both MDSCs and TILs identified significant changes in immune-related pathways. In summary, addition of ENT to ICI significantly altered infiltration and function of innate immune cells, allowing for a more robust adaptive immune response. These findings provide a rationale for combination therapy in patients with immune-resistant tumors, including breast and pancreatic cancers.

2018-10-10 | GSE121030 | GEO

Transcriptome comparison of PMN-MDSCs and and normal neutrophils

Project description:Polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), also named pathologically activated neutrophil, is a critical component of tumor microenvironment (TME), playing crucial roles in tumor progression and therapy resistance. Here, we compared the transcriptome of PMN-MDSCs from B16 tumor bearing mice and the neutrophils from tumor free mice.

2023-06-26 | GSE199601 | GEO

Gene expression data from the tumor cell supernatant-induced MDSCs

Project description:Myeloid derived suppressor cells (MDSCs) markedly expand and participate in the suppression of immune responses in inflammation and tumor microenvironment. It was confirmed that MDSCs could be generated in vitro from bone marrow cells (BMCs) after 4 days GM-CSF only or GM-CSF plus IL-6 treatment. To identify the regulation of MDSCs in tumor microenvironment, we analyzed the gene expression from tumor cell ID8 supernant-induced MDSCs compared to BMCs.

2016-12-13 | GSE92303 | GEO

RNA-Seq of myeloid derived suppressor cells (MDSCs) from wild-type and Rel knockout mice

Project description:Bone marrow-derived MDSCs were generated from bone marrow of naive WT or Rel-/- mice. After red blood cell lysis, BM cells were cultured in complete RPMI medium containing GM-CSF (100 ng/mL) and IL-6 (100 ng/mL) for 7 days. RNAs were collected afterwards for RNA-Seq.

2020-03-10 | E-MTAB-8674 | biostudies-arrayexpress

Expression data from MDSCs at different time points during tumor progression

Project description:Myeloid-derived suppressor cells (MDSCs) are increased by tumor-derived factors and suppress anti-tumor immunity. MDSCs obtained at a late time point after tumor injection had stronger suppressive activity than MDSCs obtained at an early time point, as measured by T cell proliferation assays. To find factors in MDSCs that change during tumor growth, we analyzed gene expression profiles from MDSCs at different time points after tumor injection. We found that immune response-related genes were down-regulated, but pro-tumor function-related genes were up-regulated in both Mo-MDSCs and PMN-MDSCs at the late time point. Among differentially expressed genes, FK506 binding protein 51 (FKBP51), which is a member of the immunophilin protein family and plays a role in immunoregulation, was increased in the Mo- and PMN-MDSCs isolated from the late time points. Experiments using siRNA and a chemical inhibitor of FKBP51 revealed that FKBP51 contributes to the regulation of the suppressive function of MDSCs by increasing iNOS, ARG1, and ROS levels and enhancing NF-kappaB activity. Collectively, our data suggest that FKBP51 is a novel molecule that can be targeted to regulate the immunosuppressive function of MDSCs. To identify the factors that licensed MDSCs to be more suppressive as tumors grow, we analyzed gene expression profiles in the two subsets of MDSCs at different time points (3wks, 6wks) during tumor progression. CD11b+Ly-6C(high)Ly-6G(low) Mo-MDSCs and CD11b+Ly-6C(low)Ly-6G(high) PMN-MDSCs were sorted from pooled spleens of naÃ¯ve mice and Her-2/CT26 tumor-bearing mice. Total RNA was purified and gene expression was analyzed by the Affymetrix GeneChipÂ® Mouse Gene 1.0 ST Array.

2012-03-29 | E-GEOD-35398 | biostudies-arrayexpress

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