首页> 美国卫生研究院文献>PLoS Clinical Trials >Up-regulated miR155 Reverses the Epithelial-mesenchymal Transition Induced by EGF and Increases Chemo-sensitivity to Cisplatin in Human Caski Cervical Cancer Cells
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Up-regulated miR155 Reverses the Epithelial-mesenchymal Transition Induced by EGF and Increases Chemo-sensitivity to Cisplatin in Human Caski Cervical Cancer Cells

机译:上调的miR155逆转了EGF诱导的上皮-间充质转化,并增加了人类Caski宫颈癌细胞对顺铂的化学敏感性。

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摘要

The epithelial-mesenchymal transition (EMT) induced by EGF promotes cervical cancer progression; however, the mechanisms underlying the EGF-induced EMT remain unclear. In this study, we reported that miR155 overexpression suppressed EGF-induced EMT, decreased migration/invasion capacities, inhibited cell proliferation and increased the chemo-sensitivity to DDP in human Caski cervical cancer cells. Further, the overexpression of miR155 increased TP53 expression but reduced SMAD2, and CCND1 expression levels. These data suggest that miR155 negatively regulates EGF-induced EMT. We conclude that miR155 does not act as an oncogene but as a tumour suppressor in Caski cells.
机译:EGF诱导的上皮-间质转化(EMT)促进宫颈癌的进展;但是,EGF诱导的EMT的潜在机制尚不清楚。在这项研究中,我们报道了miR155过表达抑制人Caski宫颈癌细胞中EGF诱导的EMT,降低迁移/侵袭能力,抑制细胞增殖并增加了对DDP的化学敏感性。此外,miR155的过表达增加了TP53表达,但降低了SMAD2和CCND1表达水平。这些数据表明,miR155负调节EGF诱导的EMT。我们得出的结论是,miR155在Caski细胞中不充当癌基因,而充当肿瘤抑制因子。

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