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RB-loss determines selective resistance and novel vulnerabilities in breast cancer modelsRB loss

ABSTRACT: RB-loss determines selective resistance and novel vulnerabilities in breast cancer modelsRB loss

PROVIDER: PRJNA757134 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15571200.fastq.gz	Fastqsanger.gz
	SRR15571201.fastq.gz	Fastqsanger.gz
	SRR15571202.fastq.gz	Fastqsanger.gz
	SRR15571203.fastq.gz	Fastqsanger.gz
	SRR15571204.fastq.gz	Fastqsanger.gz

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RB-loss determines selective resistance and novel vulnerabilities in breast cancer modelsRB loss

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RB-loss determines selective resistance and novel vulnerabilities in breast cancer modelsRB loss

Project description:The retinoblastoma tumor suppressor (RB1) plays a critical role in coordinating multiple pathways that impact on tumor initiation, disease progression, and therapeutic responses. Here we interrogated the effect of CDK4/6 inhibitor in combination with mTOR inhibtor. Also, we interrogtaed the efffect of AURK and WEE1 inhibition in ER+ breast cacner models While the RB-pathway has been purported to exhibit multiple mutually exclusive events, only RB1 is mutually exclusive with multiple genetic events that deregulate CDK4/6 activity. Using an isogenic ER+ breast cancer model with targeted RB1 deletion, we identified gene expression features that link CDK4/6 activity and RB-dependency (CDK4/6-RB integrated signature). We also investigated the role of RB on apoptotic pathway. Single copy loss on chromosome 13q encompassing the RB1 locus is prevalent in many cancers, and is associated with reduced expression of multiple genes on 13q including RB1, and inversely related to the CDK4/6-RB integrated signature supporting a genetic cause/effect relationship. To probe the broader implications on tumor biology, we investigated genes that are positively and inversely correlated with the CDK4/6-RB integrated signature. This approach defined tumor-specific pathways that could represent new therapeutic vulnerabilities associated with RB-pathway activity.

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Project description:The retinoblastoma (RB) tumor suppressor is functionally inactivated in a wide range of human tumors where this inactivation promotes tumorigenesis in part by allowing uncontrolled proliferation. RB has been extensively studied, but its mechanisms of action in normal and cancer cells remain only partly understood. Here we describe a new mouse model to investigate the consequences of RB loss and its re-activation in vivo. In these mice, induction of shRNA molecules targeting RB for knock-down results in the development of phenotypes similar to RB knock-out mice, including the development of pituitary and thyroid tumors. Re-expression of RB leads to cell cycle arrest in cancer cells and repression of transcriptional programs driven by E2F activity. Thus, continuous RB loss is required for the maintenance of tumor phenotypes initiated by loss of RB, and this new mouse model will provide a new platform to investigate RB function in vivo.

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