Department of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, WI-53706, USA.
Department of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, WI-53706, USA.
Semin Cancer Biol. 2018 Apr;49:75-82. doi: 10.1016/j.semcancer.2017.05.008. Epub 2017 May 22.
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.
肿瘤组织会缺氧，其特征是葡萄糖摄取增加，随后发生糖酵解。高血糖会导致非酶糖基化或蛋白质糖化，从而导致晚期糖基化终产物 (AGE) 的积累。这些 AGE 分子与各自的受体（称为晚期糖基化终产物受体 (RAGE)）结合，并启动几种异常信号通路，导致糖尿病、阿尔茨海默病、动脉粥样硬化、心力衰竭和癌症等疾病的发生。近年来，人们对 AGE 在癌症进展中的作用进行了广泛研究。由于癌细胞本质上缺氧，并适应于诱导糖化的糖酵解，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 相互作用可能是一个潜在的治疗靶点。本文综述的目的是强调 AGE-RAGE 相互作用在缺氧癌细胞中的作用。
