Advanced Glycation End-Products Enhance Lung Cancer Cell Invasion and Migration |
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| Authors: | Te-Chun Hsia Mei-Chin Yin Mei-Chin Mong |
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| Affiliation: | 1Department of Respiratory Therapy, China Medical University, 40402 Taichung City, Taiwan; ;2Department of Internal Medicine, China Medical University Hospital, 40402 Taichung City, Taiwan;3Department of Nutrition, China Medical University, 40402 Taichung City, Taiwan;4Department of Health and Nutrition Biotechnology, Asia University, 41354 Taichung City, Taiwan; |
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| Abstract: | Effects of carboxymethyllysine (CML) and pentosidine, two advanced glycation end-products (AGEs), upon invasion and migration in A549 and Calu-6 cells, two non-small cell lung cancer (NSCLC) cell lines were examined. CML or pentosidine at 1, 2, 4, 8 or 16 μmol/L were added into cells. Proliferation, invasion and migration were measured. CML or pentosidine at 4–16 μmol/L promoted invasion and migration in both cell lines, and increased the production of reactive oxygen species, tumor necrosis factor-α, interleukin-6 and transforming growth factor-β1. CML or pentosidine at 2–16 μmol/L up-regulated the protein expression of AGE receptor, p47phox, intercellular adhesion molecule-1 and fibronectin in test NSCLC cells. Matrix metalloproteinase-2 protein expression in A549 and Calu-6 cells was increased by CML or pentosidine at 4–16 μmol/L. These two AGEs at 2–16 μmol/L enhanced nuclear factor κ-B (NF-κ B) p65 protein expression and p38 phosphorylation in A549 cells. However, CML or pentosidine at 4–16 μmol/L up-regulated NF-κB p65 and p-p38 protein expression in Calu-6 cells. These findings suggest that CML and pentosidine, by promoting the invasion, migration and production of associated factors, benefit NSCLC metastasis. |
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| Keywords: | CML pentosidine non-small cell lung cancer migration invasion |
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