ArticleJournal of translational medicine2026
Tumor-derived apoptotic extracellular vesicles impede hepatocarcinoma progression by disrupting mitochondrial metabolism.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundApoptosis undergoes dynamic changes during tumor progression and treatment and has complex effects on tumor development. Apoptotic cell-derived extracellular vesicles (Apo-EVs) have recently been recognized as key mediators of intercellular communication, but their role in hepatocellular carcinoma (HCC) remains unclear.
methodsWe performed a series of in vitro and in vivo experiments to investigate the effects of tumor-derived Apo-EVs on HCC cell proliferation, apoptosis, and metabolic remodeling. Additional mechanistic studies were conducted to identify the functional cargo molecules carried by Apo-EVs and to determine their roles in ATP synthesis and metabolic regulation.
resultsTumor-derived Apo-EVs suppressed HCC cell proliferation and increased apoptosis. Mechanistically, Apo-EVs promoted apoptotic cell death by shifting cellular metabolism from aerobic glycolysis to oxidative phosphorylation. Notably, transmembrane protein 70 (TMEM70), which is transported by Apo-EVs, was identified as a key mediator of this process. TMEM70 participated in ATP synthesis and contributed to metabolic reprogramming in HCC cells.
conclusionsOur study reveals a potential mechanism by which tumor-derived Apo-EVs promote apoptosis and metabolic remodeling in HCC. Apo-EV-associated TMEM70 may contribute to this process through its involvement in mitochondrial metabolism. These findings suggest that Apo-EVs and selected cargo molecules may represent promising therapeutic targets for HCC.
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