Hsia Te-Chun, Yin Mei-Chin, Mong Mei-Chin
Department of Respiratory Therapy, China Medical University, 40402 Taichung City, Taiwan.
Department of Internal Medicine, China Medical University Hospital, 40402 Taichung City, Taiwan.
Int J Mol Sci. 2016 Aug 9;17(8):1289. doi: 10.3390/ijms17081289.
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, p47(phox), 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.
研究了两种晚期糖基化终产物（AGEs）——羧甲基赖氨酸（CML）和戊糖苷对两种非小细胞肺癌（NSCLC）细胞系A549和Calu-6细胞侵袭和迁移的影响。将1、2、4、8或16μmol/L的CML或戊糖苷加入细胞中。检测细胞的增殖、侵袭和迁移情况。4 - 16μmol/L的CML或戊糖苷促进了两种细胞系的侵袭和迁移，并增加了活性氧、肿瘤坏死因子-α、白细胞介素-6和转化生长因子-β1的产生。2 - 16μmol/L的CML或戊糖苷上调了受试NSCLC细胞中AGE受体、p47(phox)、细胞间黏附分子-1和纤连蛋白的蛋白表达。4 - 16μmol/L的CML或戊糖苷增加了A549和Calu-6细胞中基质金属蛋白酶-2的蛋白表达。2 - 16μmol/L的这两种AGE增强了A549细胞中核因子κ-B（NF-κB）p65蛋白表达和p38磷酸化。然而，4 - 16μmol/L的CML或戊糖苷上调了Calu-6细胞中NF-κB p65和p-p38蛋白表达。这些发现表明，CML和戊糖苷通过促进侵袭、迁移及相关因子的产生，有利于NSCLC转移。
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