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首页> 外文期刊>Cell communication & adhesion >Combined interferon-gamma and tumor necrosis factor-alpha treatment differentially affects adhesion and migration of keratinocyte-derived cells to laminin-1
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Combined interferon-gamma and tumor necrosis factor-alpha treatment differentially affects adhesion and migration of keratinocyte-derived cells to laminin-1

机译：干扰素-γ和肿瘤坏死因子-α的联合治疗差异性影响角质形成细胞来源的细胞向层粘连蛋白-1的粘附和迁移

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Interactions with the extracellular matrix constitute basic steps in cervix carcinoma cell invasion. In this study, we examined the adhesion and migration profiles of two human papillomavirus (HPV) DNA-transfected keratinocyte-derived cell lines, EIL8 and 18-1 1S3, and of the cervix adenocarcinoma SiHa cell line, towards laminin-1, and the selective effect of a 24-72h treatment of 1000 U/ml interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha(TNF-alpha), a treatment that significantly decreases cervix carcinoma cell proliferation and progression in nude mice, on these parameters. Compared to normal cervix keratinocytes (CK) and two HPV DNA-transfected keratinocyte cell lines, in basal conditions, the SiHa cell line was characterized by increased attachment (SiHa, 48.74 +/- 4.02 vs. normal keratinocytes, 4.32 +/- 0.40, EIL8, 17.80 +/- 3.03 and 18-1 1S3, 17.82 +/- 1.48% of attached cells after 30 min) and marked directed chemotactic migration towards laminin-1. Interestingly, treatment of the cells with the cytokines (1000 U/ml IFN-gamma and TNF-ol) did not modulate the adhesion properties of the cells, but chemotactic migration of SiHa cells to laminin-1 was significantly decreased, while migration towards type I collagen was increased. Similar results were obtained with the Ca Ski cervix carcinoma cell line. Our results emphasize the altered pattern of interactions of cervix carcinoma cells with extracellular matrix components such as laminin-1, compared to normal and preneoplastic cells, and contributes to the understanding of the effects of cytokine treatment on cervix carcinoma cells. [References: 31]
机译：与细胞外基质的相互作用构成宫颈癌细胞侵袭的基本步骤。在这项研究中，我们研究了两种人类乳头瘤病毒（HPV）DNA转染的角质形成细胞衍生的细胞系EIL8和18-1 1S3，以及子宫颈腺癌SiHa细胞系对层粘连蛋白1和在24至72小时内治疗1000 U / ml干扰素-γ（IFN-γ）和肿瘤坏死因子-α（TNF-α）的选择性效果，该治疗可显着降低裸鼠宫颈癌细胞的增殖和进程参数。与正常子宫颈角质形成细胞（CK）和两种HPV DNA转染的角质形成细胞系相比，在基础条件下，SiHa细胞系的特征是附着力增加（SiHa，相对于正常角质形成细胞为48.74 +/- 4.02，4.32 +/- 0.40， EIL8，17.80 +/- 3.03和18-1 1S3，在30分钟后附着细胞的17.82 +/- 1.48％），并标志着趋化趋向于层粘连蛋白1迁移。有趣的是，用细胞因子（1000 U / mlIFN​​-γ和TNF-ol）处理细胞不会调节细胞的黏附特性，但SiHa细胞向层粘连蛋白1的趋化迁移显着减少，而向细胞型迁移我胶原蛋白增加了。使用Ca Ski子宫颈癌细胞系也获得了相似的结果。我们的结果强调与正常和肿瘤前细胞相比，宫颈癌细胞与细胞外基质成分（如层粘连蛋白-1）相互作用的模式改变，并有助于了解细胞因子治疗对宫颈癌细胞的影响。 [参考：31]

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