Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer

ABSTRACT: CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer

PROVIDER: PRJNA744541 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15065546.fastq.gz	Fastqsanger.gz
	SRR15065547.fastq.gz	Fastqsanger.gz
	SRR15065647.fastq.gz	Fastqsanger.gz
	SRR15065548.fastq.gz	Fastqsanger.gz
	SRR15065648.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 81

Similar Datasets

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [ChIP-seq]

Project description:CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [ChIP-seq]

| PRJNA744543 | ENA

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [RNA-Seq]

Project description:CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [RNA-Seq]

| PRJNA744547 | ENA

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [RNA-Seq]

Project description:High-dose testosterone (high-T) treatment can effectively suppress the growth of castration-resistant prostate cancer (CRPC) in preclinical studies using patient-derived xenograft (PDX) models and in clinical trials of CRPC. However, the molecular basis for this treatment remains to be determined. In previous studies, we have shown that androgen receptor (AR) can function as a transcription repressor to suppress the expression of genes mediating DNA replication via recruitment of hypophosphorylated retinoblastoma protein (Rb). However, it is unclear how Rb globally mediates this transcriptional repressor activity of AR and contributes to the tumor-suppressive effect of high-dose androgen in CRPC.

2022-02-14 | GSE179687 | GEO

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [ChIP-seq]

2022-02-14 | GSE179684 | GEO

CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-02-14 | GSE179688 | GEO

Androgenic Effects of 11-Oxygenated Androgens in Castration-Resistant Prostate Cancer

Project description:Androgenic Effects of 11-Oxygenated Androgens in Castration-Resistant Prostate Cancer

| PRJNA1257886 | ENA

Androgenic Effects of 11-Oxygenated Androgens in Castration-Resistant Prostate Cancer

Project description:Investigations of CRPC cell models demonstrate that both 11oxygenated androgens 11Ketotestesterone (11KT) and 11-hydroxytestosterone (11OHT) drive robust AR-mediated proliferative responses and significantly modulate gene and protein expression profiles, paralleling canonical androgens. They also exhibit unique transcriptional and post-transcriptional effects that include potential AR-independent pathways. Furthermore, the AR antagonist enzalutamide effectively inhibits their androgenic actions, suggesting they are primarily AR-mediated.

2025-10-10 | GSE296144 | GEO

Different doses of androgens induce the expression of distinct gene expression programs [ChIP-Seq]

Project description:Most prostate cancers express the androgen receptor (AR), and tumor growth and progression are facilitated by exceptionally low levels of systemic or intratumorally produced androgens. Paradoxically, high dose androgens have also shown considerable efficacy in the treatment of patients with late-stage metastatic PCa. In probing the mechanisms that enable cells to recognize and respond to different levels of the same hormone, it was determined that low levels of androgens, functioning through an AR monomer, facilitates a non-genomic activation of the mTOR signaling pathway to drive proliferation. Conversely, high dose androgens facilitate the formation of AR dimers to suppress c-MYC expression, inhibit proliferation and drive a transcriptional program associated with a differentiated phenotype. These findings highlight the inherent liabilities in current approaches used to inhibit AR action in PCa and are instructive as to strategies that can be used to develop new therapeutics for this disease and other androgenopathies.

2024-07-09 | GSE262744 | GEO

Different doses of androgens induce the expression of distinct gene expression programs (RNA-Seq)

2024-07-09 | GSE247592 | GEO

Different doses of androgens induce the expression of distinct gene expression programs (ATAC-Seq)

2024-07-09 | GSE247591 | GEO