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Hemorrhage-induced NRF2 signaling in tumor-associated macrophages drives cancer growth, invasion, and immunotherapy resistance

ABSTRACT: Hemorrhage-induced NRF2 signaling in tumor-associated macrophages drives cancer growth, invasion, and immunotherapy resistance

PROVIDER: PRJNA996034 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25118716.fastq.gz	Fastqsanger.gz
	SRR25118717.fastq.gz	Fastqsanger.gz
	SRR25146892.fastq.gz	Fastqsanger.gz
	SRR25146893.fastq.gz	Fastqsanger.gz
	SRR25146894.fastq.gz	Fastqsanger.gz

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Hemorrhage-activated NRF2 in tumor-associated macrophages drives cancer growth, invasion, and immunotherapy resistance.

Project description:Microscopic hemorrhage is a common aspect of cancers, yet its potential role as an independent factor influencing both cancer progression and therapeutic response is largely ignored. Recognizing the essential function of macrophages in red blood cell disposal, we explored a pathway that connects intratumoral hemorrhage with the formation of cancer-promoting tumor-associated macrophages (TAMs). Using spatial transcriptomics, we found that NRF2-activated myeloid cells possessing characteristics of procancerous TAMs tend to cluster in perinecrotic hemorrhagic tumor regions. These cells resembled antiinflammatory erythrophagocytic macrophages. We identified heme, a red blood cell metabolite, as a pivotal microenvironmental factor steering macrophages toward protumorigenic activities. Single-cell RNA-Seq and functional assays of TAMs in 3D cell culture spheroids revealed how elevated intracellular heme signals via the transcription factor NRF2 to induce cancer-promoting TAMs. These TAMs stabilized epithelial-mesenchymal transition, enhancing cancer invasiveness and metastatic potential. Additionally, NRF2-activated macrophages exhibited resistance to reprogramming by IFN-γ and anti-CD40 antibodies, reducing their tumoricidal capacity. Furthermore, MC38 colon adenocarcinoma-bearing mice with NRF2 constitutively activated in leukocytes were resistant to anti-CD40 immunotherapy. Overall, our findings emphasize hemorrhage-activated NRF2 in TAMs as a driver of cancer progression, suggesting that targeting this pathway could offer new strategies to enhance cancer immunity and overcome therapy resistance.

| S-EPMC10849758 | biostudies-literature

NRF2-dependent ECM - Nrf2-Mediated Fibroblast Reprogramming Drives Cellular Senescence by Targeting the Matrisome

Project description:Nrf2-mediated fibroblast reprogramming drives cellular senescence by targeting the matrisome. ECM was isolated from WT and NRF2-/- mouse fibroblasts and analyzed by label-free quantification.

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GNPS - Nrf2 drives activation-driven expansion of CD4+ T-cells by modulating glucose and glutamine metabolism

Project description:Metabolomics data pertaining to "Nrf2 drives activation-driven expansion of CD4+ T-cells by modulating glucose and glutamine metabolism" manuscript

2025-07-17 | MSV000098549 | GNPS

Hemorrhage-induced NRF2 signaling in tumor-associated macrophages drives cancer growth, invasion, and immunotherapy resistance

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

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NRF2 activation in TRP53:P16 deficient mice drives oral squamous cell carcinoma

Project description:NRF2 activation in TRP53:P16 deficient mice drives oral squamous cell carcinoma

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Nrf2 drives activation-driven expansion of CD4+ T-cells by modulating glucose and glutamine metabolism

Project description:Metabolomics data pertaining to "Nrf2 drives activation-driven expansion of CD4+ T-cells by modulating glucose and glutamine metabolism" manuscript

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Fatty acid-binding protein 4 drives neuroinflammation after intracerebral hemorrhage

Project description:Fatty acid-binding protein 4 drives neuroinflammation after intracerebral hemorrhage

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Nrf2 transcript alterations

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The oncogenic action of NRF2 depends on de-glycation by Fructosamine-3-kinase (FN3K)

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RNA-seq of microglia and monocyte-derived cells in Nrf2 knockout and wild-type mice after induced intracerebral hemorrhage or sham treatment

Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). Having found that ICH is associated with activation of genes regulated by the transcription factor Nrf2, particularly in mononuclear myeloid cells (for example, monocyte-derived cells (MdC) and microglia), we sought to determine the importance of Nrf2 to mononuclear myeloid cell responses and their impact on ICH pathology. We used intrastriatal injection of collagenase to induce ICH in both wild-type mice, and knockout mice with Cx3cr1-Cre-mediated excision of Nrf2 (Nfe2l2) exon 5.

2024-08-13 | E-MTAB-14324 | biostudies-arrayexpress

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