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Overexpression of IGF-1 During Early Development Expands the Number of Mammary Stem Cells and Primes them for Transformation

ABSTRACT: Overexpression of IGF-1 During Early Development Expands the Number of Mammary Stem Cells and Primes them for Transformation

PROVIDER: PRJNA727819 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14458500_1.fastq.gz	Fastqsanger.gz
	SRR14458500_2.fastq.gz	Fastqsanger.gz
	SRR14458600_1.fastq.gz	Fastqsanger.gz
	SRR14458600_2.fastq.gz	Fastqsanger.gz
	SRR14458501_1.fastq.gz	Fastqsanger.gz

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Overexpression of IGF-1 During Early Development Expands the Number of Mammary Stem Cells and Primes them for Transformation

Project description:In this paper we report transcriptomic profiles of mammary stem cells (MaSCs) from female BK5.IGF1 transgenic and age-matched WT mice, generated by single-cell RNA-sequencing technology. We found that IGF-1 stimulated quiescent MaSCs to enter the cell cycle and increased their expression of genes involved in proliferation, plasiticity, tumorigenesis, invasion, and metastasis.

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Project description:Ewing sarcoma (EwS) is an aggressive cancer of adolescents in need of effective treatment. Insulin-like growth factor (IGF) 1 is an autocrine growth factor for EwS, but only 10% of patients responded to IGF-1 receptor blockade. Although presumed to originate from mesenchymal progenitors during bone development, targeting of the EwS driver oncogene EWS::FLI1 to the mesenchymal lineage in a mouse model does not result in tumor formation but to skeletal malformations and perinatal death. We report that transient exposure to IGF-1 concentrations mimicking serum levels during puberty reprogrammes limb-derived mesenchymal cells of EWS::FLI1-mutant mice to stable transformation and tumorigenicity. We identify a modular mechanism of IGF-1-driven tumor promotion in the early steps of EwS pathogenesis, in which Yap1 plays a central role. Pharmacologic Yap1/Tead inhibition reverses the transformed phenotype of EWS::FLI1 expressing cells. Our data provide a rationale for combined IGF-1R and YAP/TEAD inhibition in the treatment of EwS patients.

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