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Regulation of the Metabolism of Polyunsaturated Fatty Acids and Butyrate in Colon Cancer Cells

机译:结肠癌细胞中多不饱和脂肪酸和丁酸代谢的调节

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摘要

Experimental and epidemiological evidence supports the idea that dietary fat and fiber influence colon carcinogenesis. Particularly, their components, n-3 polyunsaturated fatty acids (PUFAs) and butyrate, have been proven to exhibit beneficial effects on colon epithelial cell metabolism, signaling, and kinetics, thus preventing colon inflammation and cancer. Moreover, these effects may be strengthened by PUFA and butyrate combination. It appears that administration of these compounds might be a relatively nontoxic form of supportive therapy improving cancer treatment outcomes and slowing down or preventing recurrence of certain types of cancer. However, their efficient application has to be based on solid scientific evidence of their mechanisms of action from the molecular and cellular to the organismal level. In this review, we emphasize the role of lipids and their metabolism during tumor development, describe some important mechanisms considering cellular and molecular levels of PUFA and butyrate action in colon epithelial cells, and particularly focus on the interaction of their metabolism and the signaling pathways with respect to the differences in response of normal and cancer colon cells.
机译:实验和流行病学证据支持饮食脂肪和纤维影响结肠癌发生的观点。特别是,其成分n-3多不饱和脂肪酸(PUFA)和丁酸酯已被证明对结肠上皮细胞的代谢,信号传导和动力学表现出有益的作用,从而预防了结肠炎症和癌症。而且,PUFA和丁酸酯的组合可以增强这些作用。似乎这些化合物的给药可能是支持治疗的相对无毒的形式,可改善癌症的治疗结果并减慢或预防某些类型癌症的复发。然而,它们的有效应用必须基于其从分子和细胞到生物水平的作用机理的可靠科学证据。在这篇综述中,我们强调脂质及其代谢在肿瘤发展过程中的作用,描述了考虑细胞和分子水平的PUFA和结肠上皮细胞中丁酸作用的一些重要机制,尤其着重于脂质代谢及其与信号传导途径的相互作用。考虑到正常和结肠癌细胞反应的差异。

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