Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [scRNA-seq]

ABSTRACT: A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [scRNA-seq]

PROVIDER: PRJNA1147723 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30227934_1.fastq.gz	Fastqsanger.gz
	SRR30227934_2.fastq.gz	Fastqsanger.gz
	SRR30227935_1.fastq.gz	Fastqsanger.gz
	SRR30227935_2.fastq.gz	Fastqsanger.gz
	SRR30227936_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [scRNA-seq]

Project description:Cancers develop resistance to inhibitors of oncogenes mainly due to target-centric mechanisms such as mutations and splicing. While inhibitors or antagonists force targets to unnatural conformation contributing to protein instability and resistance, activating tumor suppressors may maintain the protein in an agonistic conformation to elicit sustainable tumor growth inhibition. Due to lack of tumor suppressor-agonists, this hypothesis and mechanisms underlying resistance are not understood. In estrogen receptor (ER)-positive breast cancer (BC), androgen receptor (AR) is a druggable tumor suppressor and offers a promising avenue for this investigation. Spatial genomics suggest that the molecular portrait of AR-expressing BC cells in tumor microenvironment corresponds to better overall patient survival, clinically confirming AR’s role as a tumor suppressor. Ligand-activation of AR-positive BC xenografts reprograms cistromes, inhibits oncogenic pathways, and promotes cellular elasticity towards a more differentiated state, while sustained treatment results in cistromes rearrangement towards transcription factor PROP1, transformation of AR into an oncogene, and activation of the JAK/STAT pathway, all culminating in lineage plasticity to an aggressive resistant subtype. While the molecular profile of AR agonist-sensitive tumors corresponds to better patient survival, the profile represented in the resistant phenotype corresponds to shorter survival. Inhibition of activated oncogenes in resistant tumors reduces growth and re-sensitizes them to AR agonists. Together, these findings indicate that persistent activation of a tumor suppressor is not fail-safe and leads to resistance through lineage plasticity-driven tumor metamorphosis. Our work provides a framework to explore the above phenomenon across multiple cancer types and underscores the importance of factoring the sensitization of tumor suppressor targets while developing agonist-like drugs

2024-10-16 | GSE274729 | GEO

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [ChIP-seq]

2024-10-16 | GSE274717 | GEO

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [RNA-seq II]

2024-10-16 | GSE274728 | GEO

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [RNA-seq I]

2024-10-16 | GSE274720 | GEO

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [AR low/high]

2024-10-16 | GSE274715 | GEO

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity

Project description:A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity

| PRJNA1147721 | ENA

JAK/STAT blockade in cHL

Project description:JAK/STAT blockade in cHL

| PRJNA770946 | ENA

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [ChIP-seq]

Project description:A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [ChIP-seq]

| PRJNA1147708 | ENA

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [RNA-seq II]

Project description:A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [RNA-seq II]

| PRJNA1147715 | ENA

A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [AR low/high]

Project description:A Molecular Switch from Tumor Suppressor to Oncogene in ER-Positive Breast Cancer: Role of Androgen Receptor, JAK-STAT, and Lineage Plasticity [AR low/high]

| PRJNA1147702 | ENA

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