Parrales Alejandro, Iwakuma Tomoo
Department of Cancer Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Int J Mol Sci. 2016 Dec 10;17(12):2074. doi: 10.3390/ijms17122074.
Enhanced proliferation and survival are common features of cancer cells. Cancer cells are metabolically reprogrammed which aids in their survival in nutrient-poor environments. Indeed, changes in metabolism of glucose and glutamine are essential for tumor progression. Thus, metabolic reprogramming is now well accepted as a hallmark of cancer. Recent findings suggest that reprogramming of lipid metabolism also occurs in cancer cells, since lipids are used for biosynthesis of membranes, post-translational modifications, second messengers for signal transduction, and as a source of energy during nutrient deprivation. The tumor suppressor p53 is a transcription factor that controls the expression of proteins involved in cell cycle arrest, DNA repair, apoptosis, and senescence. p53 also regulates cellular metabolism, which appears to play a key role in its tumor suppressive activities. In this review article, we summarize non-canonical functions of wild-type and mutant p53 on lipid metabolism and discuss their association with cancer progression.
增殖增强和存活能力提升是癌细胞的常见特征。癌细胞会发生代谢重编程,这有助于它们在营养匮乏的环境中存活。事实上,葡萄糖和谷氨酰胺代谢的改变对肿瘤进展至关重要。因此,代谢重编程如今已被广泛认可为癌症的一个标志。最近的研究结果表明,癌细胞中也会发生脂质代谢重编程,因为脂质可用于细胞膜的生物合成、翻译后修饰、信号转导的第二信使,以及在营养缺乏时作为能量来源。肿瘤抑制因子p53是一种转录因子,可控制参与细胞周期停滞、DNA修复、细胞凋亡和衰老的蛋白质的表达。p53还调节细胞代谢,这似乎在其肿瘤抑制活性中起关键作用。在这篇综述文章中,我们总结了野生型和突变型p53在脂质代谢方面的非经典功能,并讨论它们与癌症进展的关联。