A growing number of studies describe a connection between glycosphingolipids (GSLs) and glutamine metabolism, glucose metabolism and mitochondrial dysfunction in cancer cells. Since deregulated cell energy metabolism is one of cancer cells hallmarks, investigating this connection is an important step in the development of anti-cancer therapies. GSL species are often aberrantly regulated in human cancers. They cluster in signaling platforms in the plasma membrane and organelle membranes in so called glycosphingolipid enriched microdomains (GEMs), thereby regulating cell signaling pathways. The most important glutamine transporter for epithelial cells, alanine-serine-cysteine transporter 2 (ASCT2) locates in GEMs and is regulated by GEM composition. The accumulation of glucosylceramide and lactosylceramide in mitochondria associated ER membranes (MAMs) leads to increased oxidative phosphorylation. This increases mitochondrial reactive oxygen species (ROS) levels and influences mitochondrial dynamics. Here, we review current knowledge about deregulated GSL species in cancer, GSL influence on glutamine and glucose metabolism. In addition, the role of GSLs in MAMs, oxidative phosphorylation (OXPHOS) and mitochondrial dynamics with a special focus on mechanistic target of rapamycin (mTOR) signaling is discussed. mTOR seems to play a pivotal role in the connection between GSLs and glutamine metabolism as well as in mitochondrial signaling.

越来越多的研究描述了鞘糖脂（GSL）与癌细胞中的谷氨酰胺代谢，葡萄糖代谢和线粒体功能障碍之间的联系。由于细胞能量代谢失调是癌细胞的标志之一，因此研究这种联系是抗癌疗法发展的重要一步。GSL物种通常在人类癌症中受到异常调节。它们聚集在所谓的糖鞘脂富集的微区（GEM）中的质膜和细胞器膜的信号平台中，从而调节细胞信号通路。上皮细胞最重要的谷氨酰胺转运蛋白，丙氨酸-丝氨酸-半胱氨酸转运蛋白2（ASCT2）位于创业板中，并受创业板组成的监管。线粒体相关的ER膜（MAMs）中的葡萄糖基神经酰胺和乳糖基神经酰胺的积累导致氧化磷酸化增加。这会增加线粒体活性氧（ROS）水平并影响线粒体动力学。在这里，我们回顾了当前有关癌症中GSL种类失控，GSL对谷氨酰胺和葡萄糖代谢的影响的知识。此外，GSL在MAM，氧化磷酸化（OXPHOS）和线粒体动力学中的作用特别关注雷帕霉素的机械靶标（mTOR）信令进行了讨论。mTOR似乎在GSL和谷氨酰胺代谢以及线粒体信号传导之间起着关键作用。