Department of Nutritional Sciences and Rutgers Center for Lipid Research, Rutgers, the State University of New Jersey, 96 Lipman Drive, New Brunswick, NJ 08901, USA.
Cancers (Basel). 2011 May 20;3(2):2462-77. doi: 10.3390/cancers3022462.
The development and maintenance of defining features of cancer, such as unremitting cell proliferation, evasion of programmed cell death, and the capacity for colonizing local tissues and distant organs, demand a massive production of structural, signaling and energy-storing lipid biomolecules of appropriate fatty acid composition. Due to constitutive activation of fatty acid biosynthesis, cancer cell lipids are enriched with saturated (SFA) and, in particular, monounsaturated fatty acids (MUFA), which are generated by StearoylCoA desaturase-1, the main enzyme that transforms SFA into MUFA. An increasing number of experimental and epidemiological studies suggest that high levels of SCD1 activity is a major factor in establishing the biochemical and metabolic perturbations that favors the oncogenic process. This review examines evidence that suggests the critical implication of SCD1 in the modulation of multiple biological mechanisms, specifically lipid biosynthesis and proliferation and survival signaling pathways that contribute to the development and progression of cancer.
癌症的定义特征的发展和维持,如持续的细胞增殖、逃避程序性细胞死亡以及在局部组织和远处器官定植的能力,需要大量合成具有适当脂肪酸组成的结构、信号和储能脂质生物分子。由于脂肪酸生物合成的组成性激活,癌细胞脂质富含饱和脂肪酸(SFA)和单不饱和脂肪酸(MUFA),这些脂肪酸是由硬脂酰辅酶 A 去饱和酶-1 产生的,该酶主要将 SFA 转化为 MUFA。越来越多的实验和流行病学研究表明,SCD1 活性水平高是导致促进致癌过程的生化和代谢紊乱的主要因素。这篇综述检查了证据,表明 SCD1 在调节多种生物机制中的关键作用,特别是脂质生物合成以及增殖和存活信号通路,这些机制有助于癌症的发展和进展。