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PLK1 Promotes Invasion of Esophageal Squamous Cell Carcinoma Cells through Inducing Epithelial-mesenchymal Transition

机译:PLK1通过诱导上皮 - 间充质转换来促进食管鳞状细胞癌细胞的侵袭

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Polo-like kinase 1 (PLK1) has been implicated in tumorigenesis and progression. The role of PLK1 in carcinogenesis has not been fully understood. In our study, we established PLKl-overexpressed stable transfectants in esophageal squamous cell carcinoma (ESCC) cells. Ectopic overexpression of PLK1 enhanced invasiveness of ESCC cells. Compared to the empty vector-transfected cells, PLK overexpression dramatically decreased the expression of E-cadherin and increased the expression of V{TTP}8242 in PLK overexpressed ESCC cells. These data suggest that PLK1 promotes invasion of ESCC cells by inducing EMT.
机译:Polo样激酶1(PLK1)涉及肿瘤发生和进展。 PLK1在致癌物中的作用尚未得到完全理解。在我们的研究中,我们在食道鳞状细胞癌(ESCC)细胞中建立了Plkl过表达稳定转染剂。 PLK1的异位过表达增强了ESCC细胞的侵袭性。与空载体转染的细胞相比,PLK过度表达显着降低了E-Cadherin的表达,并增加了PLK过表达ESCC细胞中的V {TTP} 8242的表达。这些数据表明,PLK1通过诱导EMT来促进ESCC细胞的侵袭。

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