Metabolic regulation of the mitochondrial immune checkpoint

Abstract

Disrupting mitochondrial function in malignant cells is a promising strategy to enhance anticancer immunity. We have recently demonstrated that depriving colorectal cancer cells of serine results in mitochondrial dysfunction coupled with the cytosolic accumulation of mitochondrial DNA and consequent activation of CGAS- and STING-dependent tumor-targeting immune responses.

Keywords

• Apoptotic caspases
• BCL2
• immune checkpoint inhibition
• MOMP
• senescence
• type I interferon