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Pro-survival lipid metabolism activates intracellular complement signaling to induce inflammasome-mediated tumor metastasis

ABSTRACT: Pro-survival lipid metabolism activates intracellular complement signaling to induce inflammasome-mediated tumor metastasis

PROVIDER: PRJNA716616 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14045283_1.fastq.gz	Fastqsanger.gz
	SRR14045283_2.fastq.gz	Fastqsanger.gz
	SRR14045284_1.fastq.gz	Fastqsanger.gz
	SRR14045284_2.fastq.gz	Fastqsanger.gz
	SRR14045285_1.fastq.gz	Fastqsanger.gz

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Pro-survival lipid metabolism activates intracellular complement signaling to induce inflammasome-mediated tumor metastasis

Project description:Tumor metastasis remains one of the major causes of cancer-related deaths in patients with solid tumors. Mechanisms by which metabolic alterations regarding pro-survival lipid signaling activation in inducing cancer cell migration and metastasis are largely unknown. Here, we demonstrate that S1P metabolism activates endogenous complement signaling for inducing tumor metastasis via inducing inflammasome-mediated pro-inflammation. Our studies using molecular, pharmacologic and genetic tools showed that activation of sphingosine 1-phosphate (S1P) and S1P receptor 1 (S1P/S1PR1) induces tumor metastasis via enhanced intracellular complement signaling by the regulation of the C3-PPIL1 complex and subsequent inflammasome activation in cancer cells and in vivo xenograft-derived tumors.

2022-03-23 | GSE169443 | GEO

S1PR1 Overexpression cells activates endogenous complement signaling and inflammasome to induce tumor metastasis in mice

Project description:Cancer metastasis remains one of the major causes of cancer deaths. The molecular mechanisms of pro-survival lipid signaling activation in inducing cancer cell migration and metastasis are largely unknown. Here, our RNA seq data showed that S1PR1 overexpression B16 melanoma cells injected in C57BL/6 mice via tail vein, activates endogenous complement signaling and inflammasome to induce tumor lung metastasis.

2022-04-15 | GSE172156 | GEO

S1PR1 Overexpression cells activates endogenous complement signaling and inflammasome to induce tumor metastasis in mice

Project description:S1PR1 Overexpression cells activates endogenous complement signaling and inflammasome to induce tumor metastasis in mice

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The effect of Sphingosine-1-Phosphate Receptor 1 and Complement Component 3 conditional knockouts on primary tumors in MMTV-PyMT mice.

Project description:Sphingolipid metabolism has been shown to regulate intracellular complement activation via sphingosine-1-phosphate receptor 1 (S1PR1) signaling to stimulate NLRP3 inflammasome-induced cancer metastasis. Here, the transcriptomic effects of S1PR1 and complement C3 conditional knockouts on primary tumors in MMTV-PyMT Mice were assessed.

2026-08-11 | GSE240703 | GEO

Impact of Conditional Knockout of Complement C3 and Sphingosine-1-Phosphate Receptor 1 (S1PR1) on Lung Metastasis in MMTV-PyMT Mice

Project description:Recent evidence suggests that sphingosine-1-phosphate receptor 1 (S1PR1) modulates the intracellular complement system or the complosome to induce NLRP3 inflammasome formation and the release of IL-1β through caspase-1, thereby promoting tumor metastasis. Here, we examined the transcriptomic effects of S1PR1 and complement C3 conditional knockouts on lung metastasis in MMTV-PyMT Mice, a widely used model for studying mammary tumor progression and metastasis.

2026-06-19 | GSE235593 | GEO

Intracellular complement factor H protects neurons during CNS inflammation [bulkRNA-seq]

Project description:Intracellular complement factor H protects neurons during CNS inflammation [bulkRNA-seq]

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Complement Membrane Attack Complexes Disrupt Proteostasis to Function as Intracellular Alarmins

Project description:Complement Membrane Attack Complexes Disrupt Proteostasis to Function as Intracellular Alarmins

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Intracellular complement factor H protects neurons during CNS inflammation [bulkRNA-seq]

Project description:Complement factor H (CFH) has been implicated in neuroprotection during inflammatory neurodegeneration, but its neuron-intrinsic functions remain poorly understood. Here, we performed bulk RNA sequencing of primary neuronal cultures from Cfh conditional knockout (Cfh-cKO) and control mice under basal conditions or following glutamate-induced oxidative stress. This dataset was generated to characterize transcriptional changes associated with neuronal Cfh deficiency and to identify pathways regulated by intracellular CFH during neuronal stress responses.

2026-07-28 | GSE332759 | GEO

Unanchored ubiquitin chains promote the non-canonical inflammasome via UBXN1

Project description:Ubiquitination is a major posttranslational covalent modification that regulates numerous cellular processes including inflammasome signaling. Cells also contain unanchored ubiquitin chains (polyUb) that bind protein targets non-covalently, but their physiological functions in immunity have been appreciated only recently. Here, we report that ubiquitin regulatory domain protein 1 (UBXN1) activates the noncanonical inflammasome via unanchored Lysin (K) 48- or 63-linked polyUb. UBXN1 deficiency impairs the activation of caspase-4/11, secretion of inflammasome-dependent cytokines and pyroptosis in response to intracellular lipopolysaccharide. UBXN1-deficient mice are protected from lipopolysaccharide- and cecal-ligation-and-puncture-induced sepsis, evidenced by reduced mortality and systemic inflammation, compared to UBXN1-sufficient littermates. Mechanistically, UBXN1 together with unanchored K48/63-linked polyUb bind caspase-4/11, promote their assembly and activation. Depleting cellular unanchored polyUb with recombinant ubiquitin-specific proteinase 5 (USP5) diminishes UBXN1 binding to caspase-4/11 and inflammasome signaling, while USP5 inhibitors enhance. This study identifies UBXN1 as a potential therapeutic target for sepsis and advances our knowledge on unanchored polyUb.

2026-09-09 | GSE306549 | GEO

Type I interferon signaling is required for activation of the inflammasome during Francisella infection

Project description:Francisella are pathogenic bacteria whose virulence is linked to their ability to replicate within the host cell cytosol. Entry into the macrophage cytosol activates a host protective multimolecular complex called the inflammasome to release the proinflammatory cytokines IL-1 and IL-18 and trigger caspase-1 dependent cell death. Here we show that cytosolic Francisella induce a type I interferon (IFN) response that is essential for caspase-1 activation, inflammasome mediated cell death, and release of IL-1 and IL-18. Extensive type I IFN dependent cell death resulting in macrophage depletion occurs in vivo during Francisella infection. Type I IFN is also necessary for inflammasome activation in response to cytosolic Listeria but not vacuole localized Salmonella or extracellular ATP. These results show the specific connection between type I IFN signaling and inflammasome activation, two sequential events triggered by recognition of cytosolic bacteria. To our knowledge, this is the first example of positive regulation of inflammasome activation. This connection underscores the importance of cytosolic recognition of pathogens and highlights how multiple innate immunity pathways interact before commitment to critical host responses. Keywords: murine macrophage response to Francisella tularensis subspecies novicida infection We analyzed a series of 18 MEEBO arrays on which were hybed RNA randomly amplified from bone marrow derived macrophages infected or not with WT Francisella tularensis subspecies novicida or a the mglA mutant strain GB2.

2007-05-23 | E-GEOD-7684 | biostudies-arrayexpress

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