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 inMolecular nutrition & food research Vol. 60; no. 8; pp. 1850 - 1864
Main Authors Lin, Jer-An, Wu, Chi-Hao, Lu, Chi-Cheng, Hsia, Shih-Min, Yen, Gow-Chin
Format Journal Article
LanguageEnglish
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.
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
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– sequence: 2
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  surname: Wu
  fullname: Wu, Chi-Hao
  organization: School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan
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  givenname: Chi-Cheng
  surname: Lu
  fullname: Lu, Chi-Cheng
  organization: Department of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan
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  givenname: Shih-Min
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  fullname: Hsia, Shih-Min
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  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
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Issue 8
Keywords AGEs
RAGE
Dicarbonyls
ROS
Cancer
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2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
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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
URI https://api.istex.fr/ark:/67375/WNG-TKJC0Q9D-4/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fmnfr.201500759
https://www.ncbi.nlm.nih.gov/pubmed/26774083
https://www.proquest.com/docview/1811844061
https://www.proquest.com/docview/1815701405
https://www.proquest.com/docview/2000292811
Volume 60
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