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Extra centrosomes induce PIDD1-mediated inflammation and Immunosurveillance

ABSTRACT: Extra centrosomes induce PIDD1-mediated inflammation and Immunosurveillance

PROVIDER: PRJNA984619 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24949512.fastq.gz	Fastqsanger.gz
	SRR24949513.fastq.gz	Fastqsanger.gz
	SRR24949514.fastq.gz	Fastqsanger.gz
	SRR24949515.fastq.gz	Fastqsanger.gz
	SRR24949516.fastq.gz	Fastqsanger.gz

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Extra centrosomes induce PIDD1-mediated inflammation and Immunosurveillance

Project description:Unscheduled increases in cellular ploidy underlie defects in tissue function, premature aging, and malignancy. A concomitant event to polyploidization is the amplification of centrosomes, the main microtubule organization center in animal cells. Supernumerary centrosomes are frequent in tumors, correlating with higher aggressiveness and poor prognosis. However, extra centrosomes also exert an onco-protective effect by activating the p53 network and eliciting cell cycle arrest. Here, we report that extra centrosomes, arising during unscheduled polyploidization or aberrant centriole biogenesis, induce activation of NF-κB signaling and sterile inflammation. This signaling requires the NEMO-PIDDOsome, a multi-protein complex composed of PIDD1, RIPK1, and NEMO/IKKγ. Remarkably, the presence of supernumerary centrosomes suffices to induce a paracrine chemokine and cytokine profile, able to polarize macrophages into a pro-inflammatory phenotype. Furthermore, extra centrosomes, accumulating after cytokinesis failure, increase immunogenicity of cancer cells and render them more susceptible to NK-cell attack. Hence, extra centrosomes, the PIDDosome acts as a dual effector, able to engage not only the p53 network for cell cycle control but also NF-κB signaling to instruct innate immunity.

2023-08-21 | GSE235120 | GEO

Extra centrosomes induce PIDD1-mediated inflammation and immunosurveillance

Project description:Unscheduled increases in ploidy underlie defects in tissue function, premature aging, and malignancy. A concomitant event to polyploidization is the amplification of centrosomes, the main microtubule organization centers in animal cells. Supernumerary centrosomes are frequent in tumors, correlating with higher aggressiveness and poor prognosis. However, extra centrosomes initially also exert an onco-protective effect by activating p53-induced cell cycle arrest. If additional signaling events initiated by centrosomes help prevent pathology is unknown. Here, we report that extra centrosomes arising during unscheduled polyploidization or aberrant centriole biogenesis induce activation of NF-B signaling and sterile inflammation. This signaling requires the NEMO-PIDDosome, a multi-protein complex composed of PIDD1, RIPK1, and NEMO/IKK. Remarkably, the presence of supernumerary centrosomes suffices to induce a paracrine chemokine and cytokine profile, able to polarize macrophages into a pro-inflammatory phenotype. Furthermore, extra centrosomes increase the immunogenicity of cancer cells and render them more susceptible to NK-cell attack. Hence, the PIDDosome acts as a dual effector, able to engage not only the p53 network for cell cycle control but also NF-B signaling to instruct innate immunity.

| S-SCDT-10_15252-EMBJ_2023113510 | biostudies-other

Extra centrosomes induce PIDD1-mediated inflammation and immunosurveillance.

Project description:Unscheduled increases in ploidy underlie defects in tissue function, premature aging, and malignancy. A concomitant event to polyploidization is the amplification of centrosomes, the main microtubule organization centers in animal cells. Supernumerary centrosomes are frequent in tumors, correlating with higher aggressiveness and poor prognosis. However, extra centrosomes initially also exert an onco-protective effect by activating p53-induced cell cycle arrest. If additional signaling events initiated by centrosomes help prevent pathology is unknown. Here, we report that extra centrosomes, arising during unscheduled polyploidization or aberrant centriole biogenesis, induce activation of NF-κB signaling and sterile inflammation. This signaling requires the NEMO-PIDDosome, a multi-protein complex composed of PIDD1, RIPK1, and NEMO/IKKγ. Remarkably, the presence of supernumerary centrosomes suffices to induce a paracrine chemokine and cytokine profile, able to polarize macrophages into a pro-inflammatory phenotype. Furthermore, extra centrosomes increase the immunogenicity of cancer cells and render them more susceptible to NK-cell attack. Hence, the PIDDosome acts as a dual effector, able to engage not only the p53 network for cell cycle control but also NF-κB signaling to instruct innate immunity.

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Project description:Exosomes derived from hypertrophic cardiomyocytes induce inflammation in macrophages via miR-155 mediated MAPK pathway.

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Escape from Immunosurveillance in Pancreatic Cancer is Mediated by the Stromal Cell Expressing Fibroblast Activation Protein-Alpha

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