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Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [bulk RNA-seq]

ABSTRACT: Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [bulk RNA-seq]

PROVIDER: PRJNA1100970 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR28706300.fastq.gz	Fastqsanger.gz
	SRR28706303.fastq.gz	Fastqsanger.gz
	SRR28706306.fastq.gz	Fastqsanger.gz
	SRR28706307.fastq.gz	Fastqsanger.gz

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Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread

Project description:Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread

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Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [scRNA-seq]

Project description:Tumour-induced systemic accumulation and polarisation of neutrophils to an immunosuppressive phenotype is a potent driver of metastasis formation. Yet how mammary tumours reprogram granulopoiesis at the molecular level and when tumour imprinting occurs during neutrophil development remains underexplored. Here we combined single cell, chromatin and functional analyses to unravel the tumour-driven reprogramming of granulopoiesis, along with intervention studies aimed at reversing this process. We observe that mammary tumours accelerate commitment to the neutrophil lineage at the expense of lymphopoiesis and erythropoiesis without stimulating the development of a novel myeloid lineage. Moreover, tumour-directed immunosuppressive imprinting of neutrophils starts early in haematopoiesis. Treatment with anti-IL-1β normalised tumour-induced granulopoiesis, reduced neutrophil production of T cell suppressive superoxides and mitigated metastatic spread. Together, these data provide molecular insights into the aberrant tumour-driven neutrophil differentiation pathway leading to metastasis-promoting chronic inflammation and how it can be reversed to reduce metastatic spread.

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Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [ATAC-seq]

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Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [bulk RNA-seq]

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Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [ATAC-seq]

Project description:Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [ATAC-seq]

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Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [scRNA-seq]

Project description:Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread [scRNA-seq]

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Understanding and reversing mammary tumour-driven reprogramming of myelopoieisis to reduce metastatic spread

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

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Feed-forward Cysteine Regulation Maintains Melanoma Differentiation State and Limits Metastatic Spread

Project description:The inherent ability of melanoma cells to alter the differentiation-associated transcriptional repertoire to evade treatment and facilitate metastatic spread is well accepted and has been termed phenotypic switching. However, how these facets of cellular behavior are controlled remains largely elusive. Here we show that cysteine availability, whether from lysosomes (CTNS-dependent) or exogenously derived (SLC7A11-dependent or as N-acetylcysteine), controls melanoma differentiation-associated pathways by acting on the melanocyte master regulator MITF. Functional data indicate that low cysteine availability reduces MITF levels and impairs lysosome functions, which affects tumor ferroptosis sensitivity but improves metastatic spread in vivo. Mechanistically, cysteine-restrictive conditions reduce acetyl-CoA levels to decrease p300-mediated H3K27 acetylation at the melanocyte-restricted MITF promoter, thus forming a cysteine feed-forward regulation that controls MITF levels and downstream lysosome functions. These findings collectively suggest that cysteine homeostasis governs melanoma differentiation by maintaining MITF levels and lysosome functions, which protect against ferroptosis and limit metastatic spread.

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