Hypoxia driven glycation: Mechanisms and therapeutic opportunities.
Hypoxia driven glycation: Mechanisms and therapeutic opportunities.
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DOI：
10.1016/j.semcancer.2017.05.008
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发表时间：
2018-04
影响因子：
14.5
通讯作者：
Mukhtar H
中科院分区：
文献类型：
--
作者：
Khan MI;Rath S;Adhami VM;Mukhtar H
肿瘤肿块缺乏氧气，其特征是葡萄糖摄取增强，随后发生糖酵解。葡萄糖水平升高会导致蛋白质的非酶糖基化或糖基化，从而导致晚期糖基化终末产物(AGE)的积累。这些AGE分子与它们各自的受体结合，称为晚期糖基化终产物受体(RAGE)，并启动几个异常信号通路，导致糖尿病、阿尔茨海默氏症、动脉粥样硬化、心力衰竭和癌症等疾病的发生。近年来，年龄在癌症进展中的作用被广泛研究。由于癌细胞本质上是低氧的，并适应糖酵解，从而诱导糖基化，因此需要更详细地了解其影响。由于AGE-RAGE信号参与癌症进展，抑制AGE-RAGE相互作用可能成为潜在的治疗靶点。本综述的目的是强调年龄-RAGE相互作用在低氧癌细胞中的作用。
Tumor masses are deprived of oxygen and characterized by enhanced glucose uptake followed by glycolysis. Elevated glucose levels induce non-enzymatic glycosylation or glycation of proteins which leads to accumulation of advanced glycation end products (AGE). These AGE molecules bind to their respective receptors called the receptor for advanced glycation end products (RAGE) and initiate several aberrant signaling pathways leading to onset of diseases such as diabetes, Alzheimer’s, atherosclerosis, heart failure and cancer. The role of AGE in cancer progression is being extensively studied in recent years. As cancer cells are hypoxic in nature and adapted to glycolysis, which induces glycation, its effects need to be understood in greater detail. Since AGE-RAGE signaling is involved in cancer progression, inhibition of AGE-RAGE interaction could be a potential therapeutic target. The purpose of this review is to highlight the role of AGE-RAGE interaction in hypoxic cancer cells.
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影响因子：
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