Department of Medicine, Stony Brook University, Stony Brook, NY.
Stony Brook Cancer Center, Stony Brook University, Stony Brook, NY.
J Lipid Res. 2018 Nov;59(11):2116-2125. doi: 10.1194/jlr.M088187. Epub 2018 Aug 28.
Ceramidases hydrolyze ceramides into sphingosine and fatty acids, with sphingosine being further metabolized into sphingosine-1-phosphate (S1P); thus, ceramidases control the levels of these bioactive sphingolipids in cells and tissues. Neutral ceramidase (nCDase) is highly expressed in colorectal tissues, and a recent report showed that nCDase activity is involved in Wnt/β-catenin signaling. In addition, the inhibition of nCDase decreases the development and progression of colorectal tumor growth. Here, to determine the action of nCDase in colorectal cancer cells, we focused on the subcellular localization and metabolic functions of this enzyme in HCT116 cells. nCDase was found to be located in both the plasma membrane and in the Golgi apparatus, but it had minimal effects on basal levels of ceramide, sphingosine, or S1P. Cells overexpressing nCDase were protected from the cell death and Golgi fragmentation induced by C6-ceramide, and they showed reduced levels of C6-ceramide and higher levels of S1P and sphingosine. Furthermore, compartment-specific metabolic functions of the enzyme were probed using C6-ceramide and Golgi-targeted bacterial SMase (bSMase) and bacterial ceramidase (bCDase). The results showed that Golgi-specific bCDase also demonstrated resistance against the cell death stimulated by C6-ceramide, and it catalyzed the metabolism of ceramides and produced sphingosine in the Golgi. Targeting bSMase to the Golgi resulted in increased levels of ceramide that were attenuated by the expression of nCDase, also supporting its ability to metabolize Golgi-generated ceramide. These results are critical in understanding the functions of nCDase actions in colorectal cancer cells as well as the compartmentalized pathways of sphingolipid metabolism.
神经酰胺酶将神经酰胺水解为神经鞘氨醇和脂肪酸,神经鞘氨醇进一步代谢为神经鞘氨醇-1-磷酸(S1P);因此,神经酰胺酶控制细胞和组织中这些生物活性神经鞘脂的水平。中性神经酰胺酶(nCDase)在结直肠组织中高度表达,最近的一份报告显示,nCDase 活性参与了 Wnt/β-catenin 信号通路。此外,nCDase 的抑制可减少结直肠肿瘤生长的发展和进展。在这里,为了确定 nCDase 在结直肠癌细胞中的作用,我们专注于该酶在 HCT116 细胞中的亚细胞定位和代谢功能。发现 nCDase 位于质膜和高尔基体中,但对神经酰胺、神经鞘氨醇或 S1P 的基础水平几乎没有影响。过表达 nCDase 的细胞可免受 C6-神经酰胺诱导的细胞死亡和高尔基体碎片化的影响,并且它们显示出较低水平的 C6-神经酰胺和较高水平的 S1P 和神经鞘氨醇。此外,使用 C6-神经酰胺和靶向高尔基体的细菌鞘氨醇酶(bSMase)和细菌神经酰胺酶(bCDase)探测了该酶的特定于隔室的代谢功能。结果表明,高尔基体特异性 bCDase 也对 C6-神经酰胺刺激的细胞死亡具有抗性,并且它催化神经酰胺的代谢并在高尔基体中产生神经鞘氨醇。将 bSMase 靶向高尔基体会导致神经酰胺水平升高,而 nCDase 的表达会减弱这种升高,这也支持了它代谢高尔基体产生的神经酰胺的能力。这些结果对于理解 nCDase 在结直肠癌细胞中的作用以及神经鞘脂代谢的隔室化途径的功能至关重要。