4 research outputs found

    Dex-IR induced H1650 cell cycle arrest.

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    <p>(A) Cell cycle analysis following drug treatment for 72 h. The bar graph of the results of the cell cycle analysis of drug-treated H1650 cells shows the percentages of cells in different phases of the cell cycle (G<sub>0</sub>/G<sub>1</sub>, S, and G<sub>2</sub>/M). The bar graph shows the mean ± SEM of three independent experiments (*<i>P</i> < 0.05 <i>vs</i>. G<sub>0</sub>/G<sub>1</sub> phase in the medium; <sup>#</sup><i>P</i> < 0.05 <i>vs</i>. S phase in the medium; and <sup>§</sup><i>P</i> < 0.05 <i>vs</i>. G2/M phase in the medium). (B) Cell lysates were analyzed by Immunoblot analysis using specific antibodies against the cyclins A2, D1, B1 and Phospho-Rb. Protein loading was normalized based on GAPDH. (C) Cells were treated with 400 nM nocodazole for 24 h, and then further treated with Dex or Dex-IR for 24 h. They were then harvested, and subjected to cell cycle analysis. The bar graph shows the mean ± SEM of three independent experiments (*P < 0.05 vs. G<sub>0</sub>/G<sub>1</sub> phase in the Nocodazole).</p

    Dex-IR inhibits the invasiveness of H1650 cells.

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    <p>(A) Invasion assay of H1650 cells treated with the drugs as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0194341#pone.0194341.g001" target="_blank">Fig 1</a>. The Transwell invasion assay showed that Dex-IR suppressed the invasion of H1650 cells. Images were captured at a magnification of 400× (A, left panel). Scale bars, 100 μm. Graphical representation of the number of invasive H1650 cells per microscopic field. Each column and bar shows the SEM from three independent experiments (*<i>P</i> < 0.05 <i>vs</i>. vehicle) (A, right panel). (B) Inhibition of MMP9 activity in conditioned medium from H1650 cells treated with Dex-IR at the indicated concentration and incubated for 18 h was evaluated using gelatin zymography. Representative data from a single experiment are shown. The left lanes are standard markers. (C) qRT-PCR analysis of the MMP2, MMP9, integrin α2, and integrin α5 gene expression in cells 6 h after treatment with drugs. Each experiment was repeated three times and the results shown are representative of the three independent experiments. The bar graph shows the mean ± SEM of three independent experiments (*P < 0.05 vs. MMP2 expression in vehicle; <sup>#</sup>P < 0.05 vs. MMP9 expression in vehicle; <sup>§</sup>P < 0.05 vs. integrin α2 expression in vehicle).</p

    Ionizing-radiation-irradiated Dex (Dex-IR) inhibits the proliferation of non-small cell lung cancer (NSCLC) cells.

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    <p>(A) The chromatograms of Dex (top) and the fraction of crude extracts with Dex-IR (bottom). The chromatography conditions are given in the Materials and Methods. The arrows indicate the retention time of each peak. (B) Lung cancer cell lines were treated with increasing concentrations of Dex and Dex-IR for 24 h. The effects of Dex-IR at the indicated concentration on the viability of lung cancer cells were determined using the MTT assay and were compared with those of Dex-treated cells. Data are presented as the mean ± standard error of the mean (SEM) of three independent experiments (*<i>P</i> < 0.05). (C) H1650 cells were treated with vehicle (1% DMSO), Dex (100 ug/mL), Dex-IR (100 ug/mL), or doxorubicin (DOXO; 1 μM) for 72 h. DOXO was used as a positive control. Cells were observed using phase-contrast microscopy (40× magnification). The scale bar is 200 μm.</p