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Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression

ABSTRACT: Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression

PROVIDER: PRJNA1128796 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29477300.fastq.gz	Fastqsanger.gz
	SRR29429014.fastq.gz	Fastqsanger.gz
	SRR29429015.fastq.gz	Fastqsanger.gz
	SRR29429016.fastq.gz	Fastqsanger.gz
	SRR29429017.fastq.gz	Fastqsanger.gz

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Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression [scRNA-seq]

Project description:Hypoxia is a common feature of many solid tumors due to aberrant proliferation and angiogenesis that is associated with tumor progression and metastasis. Most of the well-known hypoxia effects are mediated through hypoxia-inducible factors (HIFs). Identification of the long-lasting effects of hypoxia beyond the immediate HIF-induced alterations could provide a better understanding of hypoxia-driven metastasis and potential strategies to circumvent it. Here, we uncovered a hypoxia-induced mechanism that exerts a prolonged effect to promote metastasis. In breast cancer patient-derived circulating tumor cell (CTC) lines and common breast cancer cell lines, hypoxia downregulated tumor intrinsic type I interferon (IFN) signaling and its downstream antigen presentation (AP) machinery in luminal breast cancer cells, via both HIF-dependent and HIF-independent mechanisms. Hypoxia induced durable IFN/AP suppression in certain cell types that was sustained after returning to normoxic conditions, presenting a “hypoxic memory” phenotype. Hypoxic memory of IFN/AP downregulation was established by specific hypoxic priming, and cells with hypoxic memory had an enhanced ability for tumorigenesis and metastasis. Overexpression of IRF3 enhanced IFN signaling and reduced tumor growth in normoxic, but not hypoxic, conditions. The histone deacetylase inhibitor (HDACi) entinostat upregulated IFN targets and erased the hypoxic memory. These results point to a mechanism by which hypoxia facilitates tumor progression through a long-lasting memory that provides advantages for CTCs during the metastatic cascade.

2024-06-28 | GSE270295 | GEO

Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression [RNA-Seq]

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Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression [scRNA-seq]

Project description:Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression [scRNA-seq]

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Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression [RNA-Seq]

Project description:Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression [RNA-Seq]

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Hypoxic Memory Mediates Prolonged Tumor Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression

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

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Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression

Project description:Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression

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Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression [scRNA-seq]

Project description:Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression [scRNA-seq]

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A tumor suppression role for EZH2 in Diffuse Intrinsic Pontine Glioma pathogenesis

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An intrinsic transcriptional program underlying synaptic scaling during activity suppression

Project description:Homeostatic scaling allows neurons to maintain stable activity patterns by globally altering their synaptic strength in response to changing activity levels. Suppression of activity by blocking action potentials increases synaptic strength through an upregulation of surface AMPA receptors. Although this synaptic up-scaling was shown to require transcription, the molecular nature of the intrinsic transcription program underlying this process and its functional significance have been unclear. Using RNA-seq, we identified 73 genes that were specifically upregulated in response to activity suppression. In particular, Neuronal pentraxin-1 (Nptx1) increased within 6 h of activity blockade, and knockdown of this gene blocked the increase in synaptic strength. Notably, Nptx1 induction is mediated by calcium influx through the T-type Voltage-Gated Calcium Channel, as well as two transcription factors, SRF and ELK1. Taken together, these results uncover a transcriptional program that specifically operates when neuronal activity is suppressed, to globally coordinate the increase in synaptic strength.

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Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression

Project description:Somatic chromosomal deletions are prevalent in cancer, yet their effects are poorly understood. The most prominent homozygous deletions affect chromosome 9p21.3 and eliminate the CDKN2A/B tumor suppressor genes, thus disabling a cell intrinsic barrier to tumorigenesis. However, half of 9p21.3 deletions encompass a cluster of 16 type I interferons (IFNs) whose co-deletion remains unexplored. To functionally dissect 9p21.3 and other genomic deletions, we developed MACHETE (Molecular Alteration of Chromosomes with Engineered Tandem Elements), a genome engineering strategy that enables flexible modeling of megabase-sized deletions. Applying MACHETE to a syngeneic mouse model of pancreatic cancer, we show that concomitant loss of the IFN cluster with Cdkn2a/b enhanced immune evasion, metastasis, and immunotherapy resistance compared to Cdkn2a/b deletions alone. Mechanistically, IFN co-deletion disrupted type I IFN signaling in the tumor microenvironment, leading to marked changes in infiltrating immune cells and escape from CD8+ T cell surveillance, effects largely driven by the poorly understood interferon epsilon (Ifne). These results reveal how IFN-encompassing 9p21.3 deletions disable cell intrinsic and extrinsic tumor suppression, thereby providing a pervasive route for immune evasion, metastasis, and immunotherapy resistance. Our study provides a framework for interrogating large deletion events in cancer and beyond.

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