Mini-reviewPotential of glycative stress targeting for cancer prevention

- Endogenous and exogenous AGEs induce glycative stress that may promote cancer onset.
- Dicarbonyls and AGEs modify cell function and tissue microenvironment.
- AGE-RAGE signalling mediates inflammation, oxidative stress, autophagy and apoptosis.
- Anti-glycating agents, RAGE and glyoxalase-1 inhibitors are proposed for cancer therapy.

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.