5 research outputs found

    Correlation of IL-17A expression with clinicopathological features in 50 cervical cancer patients.

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    <p>*Partial data unavailable, statistics was done on the available data.</p><p>Correlation of IL-17A expression with clinicopathological features in 50 cervical cancer patients.</p

    Effects of p38 inhibitor (SB203580, SB), NF-κB inhibitor (PDTC), and IL-17A on cell invasion and MMP2, MMP9 expression in cervical cancer cells.

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    <p>C33A(<b>A</b>) and Caski(<b>E</b>) cells were pretreated with SB (20 µM) and PDTC for 30 min, then incubated in the presence or absence of IL-17A (50 ng/mL) for 24 h. The cell invasive abilities were performed by Boyden chamber invasion assay. The percentage of invasive rate of C33A(<b>B</b>) and Caski(<b>F</b>) cells was expressed as a percentage of control. C33A(<b>C, D</b>) and Caski(<b>G, H</b>) cells were treated and then subjected to western blot to analyze the protein levels of MMP2, MMP 9. Values are represented as means ± SD of three independent experiments performed in triplicate. * <i>p</i><0.05 and ** <i>p</i><0.01 compared with control group respectively.</p

    IL-17A can activate p38 and NF-κB signal pathways in cervical cancer cells.

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    <p>Expression of p38 and p-p38 were detected by western blot analysis in C33A(<b>A</b>) and Caski(<b>E</b>) cells treated with or without IL-17A for 24 hours. Quantification of the protein levels of p38 and p-p38 in C33A(<b>B</b>) and Caski(<b>F</b>). Values are represented as means ± SD of three independent experiments performed in triplicate. *p<0.05 and **p<0.01 compared with control group, respectively. Western blot analysis was used to detect nuclear p50 and p65 expression in C33A(<b>C</b>) and Caski(<b>G</b>) cells treated with IL-17A (50 ng/mL) at indicated time points. Quantification of the nuclear protein levels of p50 and p65 in C33A(<b>D</b>) and Caski(<b>H</b>) cells. Values are represented as means ± SD of three independent experiments performed in triplicate. * <i>p</i><0.05 and ** <i>p</i><0.01 compared with control group respectively.</p

    IL-17A promoted cervical cancer cells migration and invasion.

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    <p>(<b>A, B</b>) Compared with control group cells, IL-17A treated cervical cancer cells (HeLa, C33 A, and Caski) showed higher motility in a wound-healing assay. (<b>C</b>) By cell invasive assay, the effect of IL-17A on cell invasion was detected (magnification 100×). (<b>D</b>) Total invasive cell number in each chamber was summarized. Values are represented as means ± SD of three independent experiments performed in triplicate. * <i>p</i><0.05 and ** <i>p</i><0.01 compared with control group respectively.</p

    IL-17A upregulated MMPs expression and activity and downregulated TIMP expression.

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    <p>(<b>A</b>) MMPs expression was detected by real-time PCR analysis in the cervical cancer cells treated with and without IL-17A. (<b>B</b>) After treating with IL-17A for 24 hours, the expression of MMP2, MMP9, TIMP-1, and TIMP-2 were detected by western blot analysis in cervical cancer cells. (<b>C</b>) Quantification of the protein levels of MMP-2, MMP-9, TIMP-1, and TIMP-2. MMP2 (<b>D</b>) and MMP9 (<b>E</b>) concentrations in supernatants form cells treated with or without IL-17A were analyzed by ELISA. (<b>F</b>) The effects of IL-17A on the activities of MMP2 and MMP9 were analyzed by zymography assay. (<b>G</b>) Quantification of the activities of MMP-2 and MMP-9. Values are represented as means ± SD of three independent experiments performed in triplicate. * <i>p</i><0.05 and ** <i>p</i><0.01 compared with control group respectively.</p
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