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PD-L1 drives metabolic reprogramming and mitochondrial remodeling in NSCLC cells

ABSTRACT: Tumor metabolism is governed by a complex network of processes that can influence immune evasion. Metabolic dysregulation in tumor cells often result in the accumulation of byproducts that suppress immune cell function. However, the role of PD-L1 in modulating tumor metabolic remains incompletely understood. Here, we report that PD-L1 expression in non-small cell lung cancer (NSCLC) cells is associated with increased endocytic activity and alters metabolic flux, particularly within the mitochondrial tricarboxylic acid (TCA) cycle. PD-L1 expression correlates with enhanced mitochondrial fusion and reduced fission, accompanied by changes in the expression of mitochondrial respiratory chain components. Integrated multi-omics analyses further reveal that PD-L1 is linked to alterations in histone methylation, including modifications at the PTPRN2 locus. PD-L1 expression is associated with metabolic reprogramming, altered mitochondrial dynamics, and changes in epigenetic marks.

ORGANISM(S): Homo sapiens

PROVIDER: GSE330687 | GEO | 2026/05/17

REPOSITORIES: GEO

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