Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq genome-wide maps of nuclear receptor RORγ chromatin state in the liver of pig exposed to mycotoxin

ABSTRACT: ChIP-seq genome-wide maps of nuclear receptor RORγ chromatin state in the liver of pig exposed to mycotoxin

PROVIDER: PRJNA701179 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

ChIP-seq genome-wide maps of nuclear receptor RORγ chromatin state in the liver of pig exposed to mycotoxin

Project description:We show that RORγ functions as a master activator of the entire mevalonate pathway-cholesterol biosynthesis program in the porcine liver. RORγ genome-wide binding enrichments in the liver were significantly reduced in response to mycotoxin exposure.

2024-02-01 | GSE166520 | GEO

RORγ modulates the extracellular matrix to facilitate hepatocellular carcinoma growth and metastasis

Project description:Approximately 80%-90% of hepatocellular carcinomas (HCC) occur in a premalignant environment of fibrosis and abnormal extracellular matrix (ECM), predicting an essential role of abnormal matrix in the tumorigenesis and progress of HCC. However, the determinants of ECM in HCC are poorly defined. Here, we show that nuclear receptor RORγ is highly expressed and amplified in HCC tumors. RORγ functions as an essential activator of the matrisome program via directly driving the expression of major ECM genes in HCC cells. The elevated RORγ increased Fibronectin-1 deposition, cell-matrix adhesion, collagen production and cross-linkling, creating a favorable microenvironment to boost liver cancer metastasis. Moreover, RORγ antagonists effectively inhibit tumor growth and metastasis via ECM remodeling in multiple HCC xenografts and immune-intact models, and they effectively sensitize HCC tumors to sorafenib therapy in mice. Notably, the elevated RORγ expression is associated with ECM remodeling and metastasis in patients with HCC. Taken together, we identify RORγ as a key player in HCC progression by remodeling ECM and as an attractive therapeutic target for advanced HCC.

2024-01-24 | GSE234660 | GEO

Tumor mitochondrial oxidative phosphorylation stimulated by the nuclear receptor RORγ represents an effective therapeutic opportunity in osteosarcoma

Project description:Osteosarcoma (OS) is the most common malignant bone tumor with a poor prognosis. The treatment strategy has remained virtually unchanged over the past 40 years. Here, we show that the nuclear receptor RORγ may serve as a potential therapeutic target in osteosarcoma. OS exhibits a hyperactivated OXPHOS program, which fuels the carbon source to promote tumor progression. We found that RORγ is overexpressed in OS tumors and is linked to hyperactivated OXPHOS. RORγ induces the expression of PGC-1β and physically interacts with it to activate the OXPHOS program by upregulating the expression of respiratory chain component genes. Knockdown or pharmacological inhibition of RORγ strongly inhibits OXPHOS activation, downregulates mitochondrial functions and increases ROS production, which results in OS cell apoptosis and ferroptosis. RORγ inverse agonists strongly suppressed OS tumor growth and progression in multiple cell-based xenograft models and in chemotherapy-resistant, patient-derived xenograft (PDX) models and sensitized OS tumors to chemotherapy without obvious toxicity in mice. Taken together, our results indicate that RORγ is a critical regulator of the OXPHOS program in OS and provide a potential therapeutic strategy for this deadly disease.

2024-04-15 | GSE261067 | GEO

Nuclear receptor RORγ is a targetable master regulator of cholesterol in a subtype of breast cancer [RNA-Seq]

Project description:We show that triple-negative breast cancer (TNBC) exhibits a hyper-activated MVA-CB program that is strongly linked to nuclear receptor RORγ, compared to estrogen receptor-positive breast cancer. Genetic and pharmacological inhibition of RORγ reduces tumor cholesterol contents and synthesis rate while preserving host cholesterol homeostasis. We demonstrate, for the first time, that RORγ functions as a master activator of the entire MVA-CB program, dominantly over SREBP2, through its own direct binding and facilitating the recruitment of SREBP2. RORγ inhibition disrupts its association with SREBP2 and reduces MVA-CB chromatin acetylation. RORγ antagonists cause sustained TNBC tumor regression in patient-derived and immune-intact models. Their combination with cholesterol-lowering statins elicits superior anti-tumor synergy selectively in TNBC. Together, our studies uncover a previously unsuspected master regulator of MVA-CB and an attractive target for TNBC.

2019-08-04 | GSE131856 | GEO

Nuclear receptor RORγ is a targetable master regulator of cholesterol in a subtype of breast cancer [ChIP-Seq]

2019-08-04 | GSE126380 | GEO

RNAseq data for chicken liver cells under mycotoxin treatment

Project description:RNAseq data for chicken liver cells under mycotoxin treatment

2019-06-21 | GSE112862 | GEO

Natural compounds ursolic acid and digoxin exhibit inhibitory activities to cancer cells in RORγ-dependent and -independent manner

Project description:Natural compounds ursolic acid (UA) and digoxin isolated from fruits and other plants display potent anti-cancer effects in preclinical studies. UA and digoxin have been at clinical trials for treatment of different cancers including prostate cancer, pancreatic cancer and breast cancer. However, they displayed limited benefit to patients. Currently, a poor understanding of their direct targets and mechanisms of action (MOA) severely hinders their further development. We previously identified nuclear receptor RORγ as a novel therapeutic target for castration-resistant prostate cancer (CRPC) and triple-negative breast cancer (TNBC) and demonstrated that tumor cell RORγ directly activates gene programs such as androgen receptor (AR) signaling and cholesterol metabolism. Previous studies also demonstrated that UA and digoxin are potential RORγt antagonists in modulating the functions of immune cells such as Th17 cells. Here we showed that UA displays a strong activity in inhibition of RORγ-dependent transactivation function in cancer cells, while digoxin exhibits no effect at clinically relevant concentrations. In prostate cancer cells, UA down-regulates RORγ-stimulated AR expression and AR signaling, whereas digoxin up-regulates AR signaling pathway. In TNBC cells, UA but not digoxin alters RORγ-controlled gene programs of cell proliferation, apoptosis and cholesterol-biosynthesis.Together, our study reveals for the first-time that UA, but not digoxin, acts as a natural antagonist of RORγ in the cancer cells. Our finding that RORγ is a direct target of UA in cancer cells will help select patients with tumors that likely respond to UA treatment.

2023-05-17 | GSE230039 | GEO

Yeast Genomic Expression Patterns in Response to glucosylated mycotoxin

Project description:The evaluation of mycotoxicity about glucosylated mycotoxin using yeast gene expression comparison analysis. Yeast BY4743 derivative PDR5 mutant was used for this study.

2015-04-01 | GSE63663 | GEO

Therapeutic targeting MDR1 expression by RORγ antagonists resensitizes cross-resistant CRPC to taxane via coordinated induction of cell death programs

Project description:We report here that RORγ, a nuclear receptor family member, unexpectedly mediates MDR1/ABCB1 overexpression. RORγ plays an important role in controlling the functions of subsets of immune cells and has been an attractive target for autoimmune diseases. We found that its small-molecule antagonists are efficacious in re-sensitizing DTX and CTX cross-resistant CRPC cells and tumors to taxanes in both androgen receptor (AR)-positive and -negative models. Our mechanistic analyses revealed that combined treatment with RORγ antagonists and taxane elicited a robust synergy in killing the resistant cells, which involves a coordinated alteration of p53, Myc and E2F-controlled programs critical for both intrinsic and extrinsic apoptosis, survival and cell growth. Our results suggest that targeting RORγ with small-molecule inhibitors is a novel strategy for chemotherapy resensitization in tumors with MDR1 overexpression.

2019-10-12 | GSE138751 | GEO

Computer Assisted Early Detection of Liver Metastases From fMRI Maps

Project description:The purpose of this protocol is to develop a detailed MRI technique and haemodynamic maps enabling early detection of colorectal metastases in the liver.

| 2037102 | ecrin-mdr-crc

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