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Resetting cancer stem cell regulatory nodes upon MYC inhibition

ABSTRACT: Resetting cancer stem cell regulatory nodes upon MYC inhibition

PROVIDER: PRJNA342114 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4188700.fastq.gz	Fastqsanger.gz
	SRR4188710.fastq.gz	Fastqsanger.gz
	SRR4188730.fastq.gz	Fastqsanger.gz
	SRR4188740_1.fastq.gz	Fastqsanger.gz
	SRR4188740_2.fastq.gz	Fastqsanger.gz

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Resetting cancer stem cell regulatory nodes upon MYC inhibition.

Project description:MYC deregulation is common in human cancer and has a role in sustaining the aggressive cancer stem cell populations. MYC mediates a broad transcriptional response controlling normal biological programmes, but its activity is not clearly understood. We address MYC function in cancer stem cells through the inducible expression of Omomyc-a MYC-derived polypeptide interfering with MYC activity-taking as model the most lethal brain tumour, glioblastoma. Omomyc bridles the key cancer stemlike cell features and affects the tumour microenvironment, inhibiting angiogenesis. This occurs because Omomyc interferes with proper MYC localization and itself associates with the genome, with a preference for sites occupied by MYC This is accompanied by selective repression of master transcription factors for glioblastoma stemlike cell identity such as OLIG2, POU3F2, SOX2, upregulation of effectors of tumour suppression and differentiation such as ID4, MIAT, PTEN, and modulation of the expression of microRNAs that target molecules implicated in glioblastoma growth and invasion such as EGFR and ZEB1. Data support a novel view of MYC as a network stabilizer that strengthens the regulatory nodes of gene expression networks controlling cell phenotype and highlight Omomyc as model molecule for targeting cancer stem cells.

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Resetting cancer stem cell regulatory nodes upon MYC inhibition

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Tumor cell-specific inhibition of MYC function using small molecule inhibitors of the HUWE1 ubiquitin ligase

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