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Regulating the expression of PDL1 is a potential tumor immunotherapy method. The expression and transport of PDL1 in the endoplasmic reticulum, nucleus, etc. have been well studied. This article elaborates on the influence of mitochondrial metabolism on the expression of PDL1. Recently, it has been discovered that the AMPK protein can directly bind to PDL1 and phosphorylate it, then accumulate in the endoplasmic reticulum, and degrade PDL1 in the endoplasmic reticulum. And AMPK is an important sensor of mitochondrial metabolic level. Disrupting mitochondrial oxidative phosphorylation and reducing the metabolic level of mitochondria can activate AMPK. Therefore, the authors hypothesized that the disruption of mitochondrial oxidative phosphorylation can achieve PDL1 degradation by activating AMPK. The authors proved this, based on which, they designed a nanomedicine to regulate mitochondrial metabolism and reshape the surface expression of PDL1 on tumor cells. Using mitochondrial-targeted dye IR-68 and mitochondrial oxidative phosphorylation interference drug clenbuterol, as well as albumin self-assembling into a nanomedicine, targeting cancer cell mitochondria, regulating oxidative phosphorylation, reducing the surface expression of PDL1 on cancer cells; at the same time, the IR-68 dye photodynamic therapy, combined treatment.
Original link:Tumor Selective Metabolic Reprogramming as a Prospective PD-L1 Depression Strategy to Reactivate Immunotherapy
