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RB depletion is required for the continuous growth of tumors initiated by loss of RB

ABSTRACT: RB depletion is required for the continuous growth of tumors initiated by loss of RB

PROVIDER: PRJNA726959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14407455_1.fastq.gz	Fastqsanger.gz
	SRR14407455_2.fastq.gz	Fastqsanger.gz
	SRR14407456_1.fastq.gz	Fastqsanger.gz
	SRR14407456_2.fastq.gz	Fastqsanger.gz
	SRR14407457_1.fastq.gz	Fastqsanger.gz

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RB depletion is required for the continuous growth of tumors initiated by loss of RB

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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RB depletion is required for the continuous growth of tumors initiated by loss of RB.

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 depletion 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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