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pubmed-article:19353243pubmed:abstractTextThis study was designed to investigate whether indomethacin and NGX6 synergistically inhibit the growth and invasiveness of human colon cancer cells (HT-29 and SW620) and to elucidate the molecular mechanism of their action. Cell proliferation was assessed by MTT assay. Cell apoptosis was assessed by acridine orange/ethidium bromide staining (AO-EB) and annexin-V-FITC/PI assay. Invasive behaviors of colorectal cancer cells were examined by cell adhesion, migration, and invasion assays. Gap junctional intercellular communication (GJIC) was assessed by the scrape-loading/dye transfer technique. The subcellular localization and expression of beta-catenin protein was examined by immunofluorescence staining and western blot analysis, respectively. Indomethacin and NGX6 had a synergistic effect on inhibiting proliferation and invasiveness of colon cancer HT-29 and SW620 cells, restoring GJIC of HT-29 and SW620, and suppressing translocation of beta-catenin from the nucleus and cytoplasm to the plasma membrane. However, they did not have synergistic effects on enhancing apoptosis and suppressing extracellular matrix adhesion of HT-29 and SW620 cells. Indomethacin and NGX6 inhibit the proliferation and invasiveness of HT-29 and SW620 colon cancer cells by attenuating the WNT/ss-catenin signaling pathway.lld:pubmed
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pubmed-article:19353243pubmed:authorpubmed-author:WangXiaoyanXlld:pubmed
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pubmed-article:19353243pubmed:dateRevised2011-10-13lld:pubmed
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pubmed-article:19353243pubmed:articleTitleSynergistic effect of indomethacin and NGX6 on proliferation and invasion by human colorectal cancer cells through modulation of the Wnt/beta-catenin signaling pathway.lld:pubmed
pubmed-article:19353243pubmed:affiliationDepartment of Digestion Medicine, The Third Affiliated Hospital of Xiang Ya School of Medicine, Central South University, Changsha, 410078, Hunan, People's Republic of China.lld:pubmed
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