Abstract
Effects of carboxymethyllysine (CML), an advanced glycation end-product (AGE), at 1, 2, 4, 8 or 16 μmol/l upon invasion and migration of A549 cells, non-small cell lung cancer (NSCLC) cells, were investigated. Results showed that CML at used test doses did not affect A549 cell growth. However, CML at 4-16 μmol/l enhanced both invasion and migration, and stimulated the release of reactive oxygen species, interleukin-6 and tumor necrosis factor-alpha in A549 cells. CML at 2-16 μmol/l increased protein expression of AGE receptor, p47<sup>phox</sup>, intercellular adhesion molecule-1, fibronectin, kappa-B (NF- κB) p65 and p-p38 in A549 cells. CML only at 4-16 μmol/l increased matrix metalloproteinase-2 expression in A549 cells. These findings indicated that CML might benefit NSCLC metastasis through promoting invasion and migration.
Highlights
Carboxymethyllysine (CML) is an advanced glycation end-product (AGE)
It is known that the activation of p38MAPK and NF-κB pathways induced the over-production of inflammatory, oxidative and/or metastatic molecules including tumor necrosis factor (TNF)-alpha, reactive oxygen species (ROS), transforming growth factor (TGF)-beta1, intercellular adhesion molecule (ICAM)-1, fibronectin and matrix metalloproteinases (MMPs) in non-small cell lung cancer (NSCLC) cells [6, 7]
Clinical evidence indicated that higher levels of TGF-beta1, ICAM-1 or MMP-2 in lung tissue were positively correlated with poor prognosis of NSCLC patients [8, 9]
Summary
Carboxymethyllysine (CML) is an advanced glycation end-product (AGE). CML and other AGEs could be detected in many processed foods including canned meats, nuts or grain products [1]. It is known that the activation of p38MAPK and NF-κB pathways induced the over-production of inflammatory, oxidative and/or metastatic molecules including tumor necrosis factor (TNF)-alpha, reactive oxygen species (ROS), transforming growth factor (TGF)-beta, intercellular adhesion molecule (ICAM)-1, fibronectin and matrix metalloproteinases (MMPs) in non-small cell lung cancer (NSCLC) cells [6, 7]. Clinical evidence indicated that higher levels of TGF-beta, ICAM-1 or MMP-2 in lung tissue were positively correlated with poor prognosis of NSCLC patients [8, 9]. The study of Takino et al [12] revealed that RAGE was correlated with cancer malignancy, and glyceraldehyde-derived AGEs promoted both migration and invasion of A549 cells, human NSCLC cells via increasing ROS generation and activating Rac 1. It is possible that the presence of AGEs from diets or endogenous bio-synthesis might up-regulate RAGE expression and activate associated pathways, which
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