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Selective Mitochondrial Respiratory Complex I Subunit Deficiency Causes Tumor Immunogenicity

ABSTRACT: Targeting of specific metabolic pathways in tumor cells has the potential to sensitize them to immune-mediated attack. Previous studies had implicated mitochondria as a potential target for cancer therapies. We screen several complex I subunit deletions for their ability to induce an immune dependent anti-tumor response. Proteomic analysis of tumors lacking the complex I subunit NDUFS4 showed an increase in proteins involved in peptide antigen processing and presentation. We determined this increase in protein levels to be driven epigenetically through H3K27 acetylation from mitochondrial derived acetyl-CoA.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Melanocyte, Melanoma Cell Line

DISEASE(S): Skin Melanoma

SUBMITTER: Pere Puigserver

LAB HEAD: Pere Puigserver

PROVIDER: PXD051275 | Pride | 2024-10-05

REPOSITORIES: Pride

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	499476_JM6752pp_jason_41921.mzIdentML	Mzid
	499477_JM6753app_jason_41921.mzIdentML	Mzid
	499478_JM6754pp_jason_41921.mzIdentML	Mzid
	JM6752.raw	Raw
	JM6752pp_jason_41921.mzXML	Mzxml

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Defective NADPH Production in Mitochondrial Disease Complex I Causes Inflammation and Cell Death

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