Interleukin-17 augments tumor necrosis factor α-mediated increase of hypoxia-inducible factor-1α and inhibits vasodilator-stimulated phosphoprotein expression to reduce the adhesion of breast cancer cells

白细胞介素-17增强肿瘤坏死因子α介导的缺氧诱导因子-1α的增加并抑制血管扩张剂刺激的磷蛋白表达以减少乳腺癌细胞的粘附

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作者:Kuang Changchun, Hu Pengchao, Su Ke, Wang Ying, Wei Lei

Abstract

Interleukin-17 (IL-17) and tumor necrosis factor (TNF)-α are able to cooperatively alter the expression levels of a number of genes. In the present study, the mRNA expression levels of hypoxia-inducible factor (HIF)-1α were analyzed in MDA-MB-231 breast cancer cells following treatment with IL-17, TNF-α or the combination of IL-17 and TNF-α. The protein expression levels of HIF-1α and vasodilator-stimulated phosphoprotein (VASP) were evaluated using western blot analysis. The adhesive ability of the cells was determined using an MTT assay following treatment with HIF-1α-small interfering RNA and short hairpin RNA-VASP that were used to suppress the expression levels of HIF-1α and VASP protein, respectively. These results demonstrated that IL-17 augmented TNF-α-induced gene expression of HIF-1α. The combination of IL-17 and TNF-α promoted an increase in HIF-1α expression and a decrease in VASP expression and a reduction in the adhesive ability of cells. These results demonstrated that IL-17 effectively enhanced the TNF-α-induced increase in HIF-1α and inhibited VASP expression, thus reducing the adhesion of MDA-MB-231 cells.

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