N-acetylasparate (NAA), previously considered a brain-specific metabolite, is found in several cancers. However, whether it plays a role in tumor growth or survival is not fully understood. We provide evidence that NAA prevents cell death in low-glucose conditions via sustaining intracellular UDP-N-acetylglucosamine (UDP-GlcNac) levels, suppressing endoplasmic reticulum (ER) stress, and enabling continued protein synthesis. NAA production is critical for in vivo tumor growth where lower glucose levels are present than those in cell culture. Furthermore, the breakdown of NAA leads to ER stress and cell death, suggesting that the role of NAA in low-glucose is independent of its catabolism to produce aspartate or acetate. Together, these data suggest NAA can support the growth of some tumors by helping them cope with glucose limitations in vivo.

中文翻译：

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葡萄糖受限时，N-乙酰天门冬氨酸可提高细胞存活率

先前被认为是脑特异性代谢产物的N-乙酰天冬氨酸（NAA）被发现于多种癌症中。然而，是否在肿瘤生长或存活中起作用尚不清楚。我们提供的证据表明，NAA可以通过维持细胞内UDP-N-乙酰氨基葡萄糖（UDP-GlcNac）水平，抑制内质网（ER）压力并实现持续的蛋白质合成来防止低血糖情况下的细胞死亡。NAA产生对于体内肿瘤生长至关重要，在体内肿瘤生长中，葡萄糖水平低于细胞培养物中的葡萄糖水平。此外，NAA的分解会导致ER应激和细胞死亡，这表明NAA在低血糖中的作用与其分解代谢无关，以产生天冬氨酸或乙酸。总之，这些数据表明NAA可以通过帮助它们应对体内葡萄糖不足而支持某些肿瘤的生长。