Metabolic flexibility is a peculiar hallmark of cancer cells. A growing number of observations reveal that tumors can utilize a wide range of substrates to sustain cell survival and proliferation. The diversity of carbon sources is indicative of metabolic heterogeneity not only across different types of cancer but also within those sharing a common origin. Apart from the well-assessed alteration in glucose and amino acid metabolisms, there are pieces of evidence that cancer cells display alterations of lipid metabolism as well; indeed, some tumors use fatty acid oxidation (FAO) as the main source of energy and express high levels of FAO enzymes. In this metabolic pathway, the cofactor carnitine is crucial since it serves as a “shuttle-molecule” to allow fatty acid acyl moieties entering the mitochondrial matrix where these molecules are oxidized via the β-oxidation pathway. This role, together with others played by carnitine in cell metabolism, underlies the fine regulation of carnitine traffic among different tissues and, within a cell, among different subcellular compartments. Specific membrane transporters mediate carnitine and carnitine derivatives flux across the cell membranes. Among the SLCs, the plasma membrane transporters OCTN2 (Organic cation transport novel 2 or SLC22A5), CT2 (Carnitine transporter 2 or SLC22A16), MCT9 (Monocarboxylate transporter 9 or SLC16A9) and ATB^{0, +} [Sodium- and chloride-dependent neutral and basic amino acid transporter B(0+) or SLC6A14] together with the mitochondrial membrane transporter CAC (Mitochondrial carnitine/acylcarnitine carrier or SLC25A20) are the most acknowledged to mediate the flux of carnitine. The concerted action of these proteins creates a carnitine network that becomes relevant in the context of cancer metabolic rewiring. Therefore, molecular mechanisms underlying modulation of function and expression of carnitine transporters are dealt with furnishing some perspective for cancer treatment.

代谢柔韧性是癌细胞的独特特征。越来越多的观察结果表明，肿瘤可以利用多种底物维持细胞存活和增殖。碳源的多样性不仅在不同类型的癌症中而且在具有共同起源的癌症中都表明代谢异质性。除了可以很好地评估葡萄糖和氨基酸代谢的改变外，还有证据表明癌细胞也表现出脂质代谢的改变。实际上，某些肿瘤利用脂肪酸氧化（FAO）作为主要能量来源，并表达高水平的FAO酶。在这个代谢途径中 辅因子肉碱至关重要，因为它是“穿梭分子”，允许脂肪酸酰基部分进入线粒体基质，在这些分子中，这些分子通过β-氧化途径被氧化。这种作用以及肉碱在细胞代谢中所起的其他作用，奠定了肉碱在不同组织之间以及细胞内不同亚细胞区室之间运输的精细调节的基础。特定的膜转运蛋白介导肉碱和肉碱衍生物流过细胞膜。在SLC中，质膜转运蛋白OCTN2（有机阳离子转运蛋白2或SLC22A5），CT2（肉碱转运蛋白2或SLC22A16），MCT9（单羧酸盐转运蛋白9或SLC16A9）和ATB 是不同组织之间以及细胞内不同亚细胞区室之间肉碱运输的精细调节的基础。特定的膜转运蛋白介导肉碱和肉碱衍生物流过细胞膜。在SLC中，质膜转运蛋白OCTN2（有机阳离子转运蛋白2或SLC22A5），CT2（肉碱转运蛋白2或SLC22A16），MCT9（单羧酸盐转运蛋白9或SLC16A9）和ATB 是不同组织之间以及细胞内不同亚细胞区室之间肉碱运输的精细调节的基础。特定的膜转运蛋白介导肉碱和肉碱衍生物流过细胞膜。在SLC中，质膜转运蛋白OCTN2（有机阳离子转运蛋白2或SLC22A5），CT2（肉碱转运蛋白2或SLC22A16），MCT9（单羧酸盐转运蛋白9或SLC16A9）和ATB^0，+ [最依赖钠和氯的中性和碱性氨基酸转运蛋白B（0+）或SLC6A14]以及线粒体膜转运蛋白CAC（线粒体肉碱/酰基肉碱载体或SLC25A20）是调解肉碱流量的最公认方法。这些蛋白质的协同作用产生了肉碱网络，该肉碱网络在癌症代谢重新连接的情况下变得相关。因此，涉及功能调节和肉碱转运蛋白表达的分子机制为癌症治疗提供了一些前景。