Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression
In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great attention for its putative effects on cancer development. AGEs are a group of compounds formed from the complex chemical reaction of reducing sugars...
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Published in | Molecular nutrition & food research Vol. 60; no. 8; pp. 1850 - 1864 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Germany
Blackwell Publishing Ltd
01.08.2016
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Abstract | In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great attention for its putative effects on cancer development. AGEs are a group of compounds formed from the complex chemical reaction of reducing sugars with compounds containing an amino group. AGEs bind to and activate the receptor for AGEs (RAGE), which is a predominant modulator of inflammation‐associated cancer, and AGEs induce reactive oxygen species that are an important regulator of the hallmarks of cancer. Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3‐deoxyglucosone and are regarded as major precursors of AGEs. These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA. Carbonylative damage then leads to many lesions, some of which are implicated in the pathogenesis of cancer. In this review, studies regarding the effects of AGEs and dicarbonyls on cancer onset or progression are systematically discussed, and the utilization of AGE inhibitors and dicarbonyl scavengers in cancer therapy are noted.
The scheme of AGEs, dicarbonyls, ROS, and inflammation in cancer onset and progression. Exogenous and endogenous AGEs/dicarbonyls induce bursts of ROS and create a chronic inflammatory state. In such conditions, AGEs, dicarbonyls, ROS and pro‐inflammatory mediators interact in a positive feedback loop, leading to cancer onset or the enhancement of cancer progression. |
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AbstractList | In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great attention for its putative effects on cancer development. AGEs are a group of compounds formed from the complex chemical reaction of reducing sugars with compounds containing an amino group. AGEs bind to and activate the receptor for AGEs (RAGE), which is a predominant modulator of inflammation-associated cancer, and AGEs induce reactive oxygen species that are an important regulator of the hallmarks of cancer. Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3-deoxyglucosone and are regarded as major precursors of AGEs. These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA. Carbonylative damage then leads to many lesions, some of which are implicated in the pathogenesis of cancer. In this review, studies regarding the effects of AGEs and dicarbonyls on cancer onset or progression are systematically discussed, and the utilization of AGE inhibitors and dicarbonyl scavengers in cancer therapy are noted. In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great attention for its putative effects on cancer development. AGEs are a group of compounds formed from the complex chemical reaction of reducing sugars with compounds containing an amino group. AGEs bind to and activate the receptor for AGEs (RAGE), which is a predominant modulator of inflammation-associated cancer, and AGEs induce reactive oxygen species that are an important regulator of the hallmarks of cancer. Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3-deoxyglucosone and are regarded as major precursors of AGEs. These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA. Carbonylative damage then leads to many lesions, some of which are implicated in the pathogenesis of cancer. In this review, studies regarding the effects of AGEs and dicarbonyls on cancer onset or progression are systematically discussed, and the utilization of AGE inhibitors and dicarbonyl scavengers in cancer therapy are noted.In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great attention for its putative effects on cancer development. AGEs are a group of compounds formed from the complex chemical reaction of reducing sugars with compounds containing an amino group. AGEs bind to and activate the receptor for AGEs (RAGE), which is a predominant modulator of inflammation-associated cancer, and AGEs induce reactive oxygen species that are an important regulator of the hallmarks of cancer. Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3-deoxyglucosone and are regarded as major precursors of AGEs. These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA. Carbonylative damage then leads to many lesions, some of which are implicated in the pathogenesis of cancer. In this review, studies regarding the effects of AGEs and dicarbonyls on cancer onset or progression are systematically discussed, and the utilization of AGE inhibitors and dicarbonyl scavengers in cancer therapy are noted. In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great attention for its putative effects on cancer development. AGEs are a group of compounds formed from the complex chemical reaction of reducing sugars with compounds containing an amino group. AGEs bind to and activate the receptor for AGEs (RAGE), which is a predominant modulator of inflammation‐associated cancer, and AGEs induce reactive oxygen species that are an important regulator of the hallmarks of cancer. Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3‐deoxyglucosone and are regarded as major precursors of AGEs. These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA. Carbonylative damage then leads to many lesions, some of which are implicated in the pathogenesis of cancer. In this review, studies regarding the effects of AGEs and dicarbonyls on cancer onset or progression are systematically discussed, and the utilization of AGE inhibitors and dicarbonyl scavengers in cancer therapy are noted. The scheme of AGEs, dicarbonyls, ROS, and inflammation in cancer onset and progression. Exogenous and endogenous AGEs/dicarbonyls induce bursts of ROS and create a chronic inflammatory state. In such conditions, AGEs, dicarbonyls, ROS and pro‐inflammatory mediators interact in a positive feedback loop, leading to cancer onset or the enhancement of cancer progression. In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great attention for its putative effects on cancer development. AGEs are a group of compounds formed from the complex chemical reaction of reducing sugars with compounds containing an amino group. AGEs bind to and activate the receptor for AGEs (RAGE), which is a predominant modulator of inflammation-associated cancer, and AGEs induce reactive oxygen species that are an important regulator of the hallmarks of cancer. Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3-deoxyglucosone and are regarded as major precursors of AGEs. These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA. Carbonylative damage then leads to many lesions, some of which are implicated in the pathogenesis of cancer. In this review, studies regarding the effects of AGEs and dicarbonyls on cancer onset or progression are systematically discussed, and the utilization of AGE inhibitors and dicarbonyl scavengers in cancer therapy are noted. The scheme of AGEs, dicarbonyls, ROS, and inflammation in cancer onset and progression. Exogenous and endogenous AGEs/dicarbonyls induce bursts of ROS and create a chronic inflammatory state. In such conditions, AGEs, dicarbonyls, ROS and pro-inflammatory mediators interact in a positive feedback loop, leading to cancer onset or the enhancement of cancer progression. |
Author | Lin, Jer-An Yen, Gow-Chin Wu, Chi-Hao Hsia, Shih-Min Lu, Chi-Cheng |
Author_xml | – sequence: 1 givenname: Jer-An surname: Lin fullname: Lin, Jer-An organization: Department of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan – sequence: 2 givenname: Chi-Hao surname: Wu fullname: Wu, Chi-Hao organization: School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan – sequence: 3 givenname: Chi-Cheng surname: Lu fullname: Lu, Chi-Cheng organization: Department of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan – sequence: 4 givenname: Shih-Min surname: Hsia fullname: Hsia, Shih-Min organization: School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan – sequence: 5 givenname: Gow-Chin surname: Yen fullname: Yen, Gow-Chin email: gcyen@nchu.edu.tw organization: Department of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26774083$$D View this record in MEDLINE/PubMed |
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Snippet | In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great... |
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SubjectTerms | advanced glycation end products AGEs Biological Factors Cancer carcinogenesis Dicarbonyls DNA Glycation End Products, Advanced - metabolism glycolysis Glycosylation lipid peroxidation lipids neoplasms Neoplasms - prevention & control Oxidation-Reduction protein degradation Pyruvaldehyde - metabolism RAGE reactive oxygen species Reactive Oxygen Species - metabolism Receptor for Advanced Glycation End Products - metabolism reducing sugars ROS therapeutics |
Title | Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression |
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