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Synthetic essentiality between PTEN and core dependency factor PAX7 dictates rhabdomyosarcoma identity

ABSTRACT: Synthetic essentiality between PTEN and core dependency factor PAX7 dictates rhabdomyosarcoma identity

PROVIDER: PRJNA702273 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13718679.fastq.gz	Fastqsanger.gz
	SRR13718679_1.fastq.gz	Fastqsanger.gz
	SRR13718679_2.fastq.gz	Fastqsanger.gz
	SRR13718680.fastq.gz	Fastqsanger.gz
	SRR13718680_1.fastq.gz	Fastqsanger.gz

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Synthetic essentiality between PTEN and core dependency factor PAX7 dictates rhabdomyosarcoma identity.

Project description:PTEN promoter hypermethylation is nearly universal and PTEN copy number loss occurs in ~25% of fusion-negative rhabdomyosarcoma (FN-RMS). Here we show Pten deletion in a mouse model of FN-RMS results in less differentiated tumors more closely resembling human embryonal RMS. PTEN loss activated the PI3K pathway but did not increase mTOR activity. In wild-type tumors, PTEN was expressed in the nucleus suggesting loss of nuclear PTEN functions could account for these phenotypes. Pten deleted tumors had increased expression of transcription factors important in neural and skeletal muscle development including Dbx1 and Pax7. Pax7 deletion completely rescued the effects of Pten loss. Strikingly, these Pten;Pax7 deleted tumors were no longer FN-RMS but displayed smooth muscle differentiation similar to leiomyosarcoma. These data highlight how Pten loss in FN-RMS is connected to a PAX7 lineage-specific transcriptional output that creates a dependency or synthetic essentiality on the transcription factor PAX7 to maintain tumor identity.

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Synthetic essentiality between PTEN and core dependency factor PAX7 dictates rhabdomyosarcoma identity

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

2021-08-24 | GSE166906 | GEO

Rhabdomyosarcoma can be initiated in activated Pax7+ Muscle Progenitor Cells

Project description:Microarray analysis of rhabdomyosarcomas generated using mice with conditional mutations in Kras and p53 using both in vivo and in vitro approaches to identify a cell of origin for rhabdomyosarcoma. Contains rhabdomyosarcomas derived in vivo using Pax7-CreER mice and in vitro using sorted muscle progenitor cells, UPS derived from intramuscular Adeno-Cre injection, and normal muscle.

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Expression data from Pax7+ satellite cell derived tumors in vitro and in vivo

Project description:Mouse muscle stem cells, defined as Pax7+ satellite cells, can initiate rhabdomyosarcoma when transformed by oncogenic Kras and concomitant loss of p53. Mouse Pax7+ satellite cells were transformed in vitro and in vivo utilizing the Cre-ER/loxp system. We wanted to address two major questions: do the in vitro and in vivo tumors cluster together compared to another mouse to another mouse derived soft-tissue sarcoma AND which human soft-tissue sarcoma do the in vivo derived tumors resemble transcriptionally? Therefore, tumors from cells transformed in vitro and tumors from mice that restrict the oncogenic lesions to Pax7+ satellite cells in vivo were compared to answer these two questions.

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Divergent transcriptional and transforming properties of PAX3-FOXO1 and PAX7-FOXO1 paralogs

Project description:Hallmarks of the alveolar subclass of Rhabdomyosarcoma are chromosomal translocations that generate PAX3-FOXO1 or PAX7-FOXO1 chimeric transcription factors. Both PAX-FOXO1s drive related cell transformation in animal models, yet the two mutations are associated with distinct pathological manifestations in patients. To evaluate the mechanisms underlying these differences, we generated isogenic fibroblast lines expressing either PAX-FOXO1 paralog. Mapping their genome recruitment using CUT&Tag revealed that the two chimeric proteins have distinct DNA binding preferences. Furthermore, PAX7-FOXO1 causes stronger de novo transactivation of its bound regions than PAX3-FOXO1, resulting in greater transcriptomic dynamics involving genes regulating cell shape and cycle. Consistently, PAX3-FOXO1 accentuates fibroblast cellular traits associated with contractility and surface adhesion and limits entry to M phase. Instead, PAX7-FOXO1 pushes cells to adopt an amoeboid-like shape, reduce S phase entry and provokes more genome instabilities. Altogether, our results demonstrate that PAX7-FOXO1 has a greater chromatin remodelling and transactivating abilities and is more deleterious to cells than PAX3-FOXO1. Altogether our results argue that the diversity in rhabdomyosarcoma manifestation stems, in part, from the diverging transcriptional activity of PAX3-FOXO1 and PAX7-FOXO1. Furthermore, PAX7-FOXO1 pronounced deleterious effects provides an explanation for the low frequency of the translocation generating this factor in Rhabdomyosarcoma patients.

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Project description:Epigenetic Lanscape and BRD4 Transcriptional Dependency of PAX3-FOXO1 Driven Rhabdomyosarcoma

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PAX3-FOXO1 expression in endothelial progenitors dictates myogenic reprogramming and rhabdomyosarcoma identity

Project description:PAX3-FOXO1 expression in endothelial progenitors dictates myogenic reprogramming and rhabdomyosarcoma identity

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Rhabdomyosarcoma can be initiated in activated Pax7+ Muscle Progenitor Cells

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PAX3-FOXO1 dictates myogenic reprogramming and rhabdomyosarcoma identity in endothelial progenitors [RNA-seq]