Potential of glycative stress targeting for cancer prevention

Christina Piperi; Christos Adamopoulos; Athanasios G. Papavassiliou

doi:10.1016/j.canlet.2017.01.020

Potential of glycative stress targeting for cancer prevention

Christina Piperi
, Christos Adamopoulos
, Athanasios G. Papavassiliou

Research output: Contribution to journal › Review article › peer-review

25 Scopus citations

Abstract

Glycative stress from endogenous and exogenous advanced glycation end-products (AGEs) has been implicated to cancer development and progression. Dicarbonyl compounds, the main AGE precursors and crosslinked AGE forms may directly react with proteins, lipids and nucleic acids, modify their structure and affect tissue microenvironment. They may also induce elevation of reactive oxygen species (ROS) and enhance cellular oxidative stress, an important regulator of cancer hallmarks. Moreover, the activation of AGE-receptor for AGE (RAGE) signalling pathways mediates inflammation, oxidative stress, autophagy and apoptosis leading to genomic instability and cancer initiation. Here, we provide evidence on the impact of glycative stress in promoting human tumorigenesis and we discuss the potential application of anti-glycating agents, RAGE and glyoxalase-1 inhibitors in cancer prevention.

Original language	English
Pages (from-to)	153-159
Number of pages	7
Journal	Cancer Letters
Volume	390
DOIs	https://doi.org/10.1016/j.canlet.2017.01.020
State	Published - 1 Apr 2017
Externally published	Yes

Keywords

AGEs
Cancer
Dicarbonyl scavengers
Glycative stress
Glyoxalase inhibitors
RAGE

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10.1016/j.canlet.2017.01.020

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title = "Potential of glycative stress targeting for cancer prevention",

abstract = "Glycative stress from endogenous and exogenous advanced glycation end-products (AGEs) has been implicated to cancer development and progression. Dicarbonyl compounds, the main AGE precursors and crosslinked AGE forms may directly react with proteins, lipids and nucleic acids, modify their structure and affect tissue microenvironment. They may also induce elevation of reactive oxygen species (ROS) and enhance cellular oxidative stress, an important regulator of cancer hallmarks. Moreover, the activation of AGE-receptor for AGE (RAGE) signalling pathways mediates inflammation, oxidative stress, autophagy and apoptosis leading to genomic instability and cancer initiation. Here, we provide evidence on the impact of glycative stress in promoting human tumorigenesis and we discuss the potential application of anti-glycating agents, RAGE and glyoxalase-1 inhibitors in cancer prevention.",

keywords = "AGEs, Cancer, Dicarbonyl scavengers, Glycative stress, Glyoxalase inhibitors, RAGE",

author = "Christina Piperi and Christos Adamopoulos and Papavassiliou, \{Athanasios G.\}",

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year = "2017",

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doi = "10.1016/j.canlet.2017.01.020",

language = "English",

volume = "390",

pages = "153--159",

journal = "Cancer Letters",

issn = "0304-3835",

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TY - JOUR

T1 - Potential of glycative stress targeting for cancer prevention

AU - Piperi, Christina

AU - Adamopoulos, Christos

AU - Papavassiliou, Athanasios G.

PY - 2017/4/1

Y1 - 2017/4/1

N2 - Glycative stress from endogenous and exogenous advanced glycation end-products (AGEs) has been implicated to cancer development and progression. Dicarbonyl compounds, the main AGE precursors and crosslinked AGE forms may directly react with proteins, lipids and nucleic acids, modify their structure and affect tissue microenvironment. They may also induce elevation of reactive oxygen species (ROS) and enhance cellular oxidative stress, an important regulator of cancer hallmarks. Moreover, the activation of AGE-receptor for AGE (RAGE) signalling pathways mediates inflammation, oxidative stress, autophagy and apoptosis leading to genomic instability and cancer initiation. Here, we provide evidence on the impact of glycative stress in promoting human tumorigenesis and we discuss the potential application of anti-glycating agents, RAGE and glyoxalase-1 inhibitors in cancer prevention.

AB - Glycative stress from endogenous and exogenous advanced glycation end-products (AGEs) has been implicated to cancer development and progression. Dicarbonyl compounds, the main AGE precursors and crosslinked AGE forms may directly react with proteins, lipids and nucleic acids, modify their structure and affect tissue microenvironment. They may also induce elevation of reactive oxygen species (ROS) and enhance cellular oxidative stress, an important regulator of cancer hallmarks. Moreover, the activation of AGE-receptor for AGE (RAGE) signalling pathways mediates inflammation, oxidative stress, autophagy and apoptosis leading to genomic instability and cancer initiation. Here, we provide evidence on the impact of glycative stress in promoting human tumorigenesis and we discuss the potential application of anti-glycating agents, RAGE and glyoxalase-1 inhibitors in cancer prevention.

KW - AGEs

KW - Cancer

KW - Dicarbonyl scavengers

KW - Glycative stress

KW - Glyoxalase inhibitors

KW - RAGE

UR - https://www.scopus.com/pages/publications/85010764200

U2 - 10.1016/j.canlet.2017.01.020

DO - 10.1016/j.canlet.2017.01.020

M3 - Review article

C2 - 28111136

AN - SCOPUS:85010764200

SN - 0304-3835

VL - 390

SP - 153

EP - 159

JO - Cancer Letters

JF - Cancer Letters

ER -

Potential of glycative stress targeting for cancer prevention

Abstract

Keywords

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