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Differential effects between amphoterin and advanced glycation end products on colon cancer cells

✍ Scribed by Hiroki Kuniyasu; Yoshitomo Chihara; Hideaki Kondo


Book ID
102269718
Publisher
John Wiley and Sons
Year
2003
Tongue
French
Weight
257 KB
Volume
104
Category
Article
ISSN
0020-7136

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✦ Synopsis


Abstract

Amphoterin is 1 ligand of the receptor for advanced glycation end products (RAGE). We studied expression of amphoterin and RAGE mRNA and proteins in colorectal carcinoma cells and investigated their associations with the invasive activities of cells exposed to advanced glycation end products (AGE). Expression of RAGE and amphoterin was examined in 4 colorectal carcinoma cell lines. All cell lines expressed both RAGE and amphoterin. The effects of RAGE and amphoterin on cell growth (MTT assay), migration (wound healing assay) and invasion (in vitro invasion assay) were tested by treatment of cells with RAGE and amphoterin antisense S‐oligodeoxynucleotides (ODNs). Cell growth, migration and invasion were inhibited significantly in Colo320 and WiDr carcinoma cells treated with RAGE and amphoterin antisense S‐ODNs compared with sense‐treated cells. Differences in ligand activity between amphoterin and AGE were examined with AGE‐bovine serum albumin (BSA). AGE‐BSA decreased cell growth, migration and invasion of amphoterin antisense S‐ODN‐treated Colo320 and WiDr cells compared with those of cells treated with Colo320 conditioned medium. Phosphorylation of extracellular signal‐regulated kinase‐1/2, Rac1 and AKT and production of matrix metalloproteinase 9 were increased to a greater degree by amphoterin than by AGE‐BSA. In contrast, production of inducible nitric oxide synthase and nuclear factor‐κBp65 were increased to a greater degree by AGE‐BSA than by amphoterin. © 2003 Wiley‐Liss, Inc.


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