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膳食碳水化合物通过上调脂肪量和肥胖相关基因的表达水平促进癌细胞存活。

Dietary Carbohydrate Promotes Cell Survival in Cancer Via the Up-Regulation of Fat Mass and Obesity-Associated Gene Expression Level.

作者信息

Doaei Saeid, Gholamalizadeh Maryam, Akbari Mohammad Esmaeil, Akbari Shayan, Feradova Hyuliya, Rahimzadeh Ghazaleh, Mosavi Jarrahi Alireza

机构信息

Student Research Committee, Cancer Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Gastrointestinal and Liver Disease Research Center, Guilan University of Medical Sciences, Rasht, Iran.

出版信息

Malays J Med Sci. 2019 Mar;26(2):8-17. doi: 10.21315/mjms2019.26.2.2. Epub 2019 Apr 30.

Abstract

Cancer cells are mainly dependent on glycolysis for their growth and survival. Dietary carbohydrates play a critical role in the growth and proliferation of cancer and a low-carbohydrate diet may help slow down the growth of tumours. However, the exact mechanisms behind this effect are unclear. This review study aimed to investigate the effect of fat mass and obesity-associated (FTO) gene in the association between dietary carbohydrates and cancer. This study was carried out using keywords such as polymorphism and/or cancer and/or dietary carbohydrate and/or FTO gene. PubMed and Science Direct databases were used to collect all related articles published from 1990 to 2018. Recent studies showed that the level of FTO gene expression in cancer cells is dramatically increased and may play a role in the growth of these cells through the regulation of the cellular metabolic pathways, including the phosphoinositide 3-kinases/protein kinaseB (PI3K/AKT) signaling pathway. Dietary carbohydrate may influence the FTO gene expression by eliminating the inhibitory effect of adenosine monophosphate-activated protein kinase (AMPK) on the FTO gene expression. This review summarised what has been recently discovered about the effects of dietary carbohydrate on cancer cells and tried to determine the mediating role of the FTO gene in these effects.

摘要

癌细胞的生长和存活主要依赖糖酵解。膳食碳水化合物在癌症的生长和增殖中起关键作用,低碳水化合物饮食可能有助于减缓肿瘤生长。然而,这种效应背后的确切机制尚不清楚。本综述研究旨在探讨脂肪量和肥胖相关(FTO)基因在膳食碳水化合物与癌症关联中的作用。本研究使用了多态性和/或癌症和/或膳食碳水化合物和/或FTO基因等关键词。利用PubMed和科学Direct数据库收集1990年至2018年发表的所有相关文章。最近的研究表明,癌细胞中FTO基因的表达水平显著升高,可能通过调节细胞代谢途径(包括磷酸肌醇3激酶/蛋白激酶B(PI3K/AKT)信号通路)在这些细胞的生长中发挥作用。膳食碳水化合物可能通过消除单磷酸腺苷激活蛋白激酶(AMPK)对FTO基因表达的抑制作用来影响FTO基因表达。本综述总结了最近关于膳食碳水化合物对癌细胞影响的发现,并试图确定FTO基因在这些影响中的介导作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a076/6687223/e05d39e83a73/02mjms26022019_ra1f1.jpg

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