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

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

PROVIDER: PRJNA744543 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15065546.fastq.gz	Fastqsanger.gz
	SRR15065547.fastq.gz	Fastqsanger.gz
	SRR15065548.fastq.gz	Fastqsanger.gz
	SRR15065549.fastq.gz	Fastqsanger.gz
	SRR15065550.fastq.gz	Fastqsanger.gz

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

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

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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]

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

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

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

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

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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.

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