Cátedra de Biología Celular, Histología y Embriología, Instituto de Biología Celular, Facultad de Ciencias Médicas CONICET-Argentina, Universidad Nacional de Córdoba, Ciudad Universitaria, Córdoba 5000, Argentina.
Cancer Metastasis Rev. 2011 Dec;30(3-4):325-42. doi: 10.1007/s10555-011-9308-x.
This article reviews the current knowledge and experimental research about the mechanisms by which fatty acids and their derivatives control specific gene expression involved during carcinogenesis. Changes in dietary fatty acids, specifically the polyunsaturated fatty acids of the ω-3 and ω-6 families and some derived eicosanoids from lipoxygenases, cyclooxygenases, and cytochrome P-450, seem to control the activity of transcription factor families involved in cancer cell proliferation or cell death. Their regulation may be carried out either through direct binding to DNA as peroxisome proliferator-activated receptors or via modulation in an indirect manner of signaling pathway molecules (e.g., protein kinase C) and other transcription factors (nuclear factor kappa B and sterol regulatory element binding protein). Knowledge of the mechanisms by which fatty acids control specific gene expression may identify important risk factors for cancer and provide insight into the development of new therapeutic strategies for a better management of whole body lipid metabolism.
这篇文章综述了脂肪酸及其衍生物控制致癌过程中特定基因表达的机制的现有知识和实验研究。饮食中脂肪酸的变化，特别是 ω-3 和 ω-6 家族的多不饱和脂肪酸以及脂加氧酶、环加氧酶和细胞色素 P-450 衍生的某些类二十烷酸，似乎控制了参与癌细胞增殖或细胞死亡的转录因子家族的活性。它们的调节可以通过作为过氧化物酶体增殖物激活受体的直接与 DNA 结合，或者通过信号转导途径分子（例如蛋白激酶 C）和其他转录因子（核因子 kappa B 和固醇调节元件结合蛋白）的间接方式进行调节。了解脂肪酸控制特定基因表达的机制可以确定癌症的重要危险因素，并为开发新的治疗策略以更好地管理全身脂质代谢提供思路。
