INSERM U858, Toulouse, France.
Autophagy. 2010 Apr;6(3):426-7. doi: 10.4161/auto.6.3.11529. Epub 2010 Apr 15.
By controlling sphingosine 1-phosphate (S1P) catabolism, S1P lyase (SPL) represents an undeniable candidate as potential regulator of a cancer cell's fate in response to stress. Our recent study reveals that complete loss of SPL activity leads to upregulation of the anti-apoptotic proteins Bcl-2 and Bcl-xL and consequently protects against apoptosis induced by chemotherapy and nutrient starvation but not against autophagy. Here, we speculate on how S1P and disruption of S1P breakdown may regulate cell death and autophagy.
通过控制鞘氨醇 1-磷酸（S1P）的分解代谢，S1P 裂解酶（SPL）作为潜在的调节剂，代表了一种不可忽视的候选物，能够调节癌细胞对压力的反应。我们最近的研究表明，SPL 活性的完全丧失会导致抗凋亡蛋白 Bcl-2 和 Bcl-xL 的上调，从而防止化疗和营养饥饿诱导的细胞凋亡，但不能防止自噬。在这里，我们推测 S1P 和 S1P 分解的破坏如何调节细胞死亡和自噬。
