Abstract：
The persistent growth of cancer cells is underscored by complex metabolic reprogramming, with mitochondria playing a key role in the transition to aerobic glycolysis and representing new therapeutic targets. Mitochondrial uncoupling protein 2 (UCP2) has attracted interest because of its abundance in rapidly proliferating cells, including cancer cells, and its involvement in cellular metabolism. However, the specific contributions of UCP2 to cancer biology remain poorly defined. Our investigation of UCP2 expression in various human and mouse cancer cell lines aimed to elucidate its links to metabolic states, proliferation, and adaptation to environmental stresses such as hypoxia and nutrient deprivation. We observed significant variability in UCP2 expression across cancer types, with no direct correlation to their metabolic activity or proliferation rates. UCP2 abundance was also differentially affected by nutrient availability in different cancer cells, but UCP2 was generally downregulated under hypoxia. These findings challenge the notion that UCP2 is a marker of malignant potential and suggest its more complex involvement in the metabolic landscape of cancer.
摘要：
复杂的代谢重编程强调了癌细胞的持续生长，线粒体在向有氧糖酵解的过渡中起着关键作用，并代表了新的治疗靶标。线粒体解偶联蛋白2（UCP2）由于其在快速增殖的细胞中的丰度而引起了人们的兴趣，包括癌细胞，以及它参与细胞代谢。然而,UCP2对癌症生物学的具体贡献尚不明确.我们研究了UCP2在各种人类和小鼠癌细胞系中的表达，旨在阐明其与代谢状态的联系。扩散,和适应环境压力，如缺氧和营养剥夺。我们观察到不同癌症类型的UCP2表达存在显著差异，与它们的代谢活动或增殖率没有直接关系。UCP2丰度也受到不同癌细胞中营养可用性的不同影响，但UCP2在缺氧条件下普遍下调。这些发现挑战了UCP2是恶性潜能的标志的观点，并表明其在癌症的代谢景观中更复杂的参与。
