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. 2019 Sep 23;39(4):767–785. doi: 10.1038/s41388-019-1023-z

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© The Author(s), under exclusive licence to Springer Nature Limited 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Loss of PLK1 activity blocks pro-tumorigenic and pro-metastatic activity induced by active PLK1 or TGF-β. a–c A549 cells were infected by lentiviral PLK1 shRNA #1 and then treated with TGF-β for 48 h. a Immunoblot analyses were performed using anti-PLK1, anti-pT210-PLK1, anti-N-cadherin, anti-E-cadherin, anti-vimentin, anti-snail, anti-slug, and anti-β−actin. b The band intensity values were quantified using LI-COR Odyssey software (Li-COR Biosciences), normalized, and plotted. c qRT-PCR was performed for PLK1, CDH1, CDH2, and VIM in A549 cells with depleted PLK1. *p < 0.05; **p < 0.01; ***p < 0.001 (n = 3). Data presented as mean ± SD. d A549 cells were infected by lentiviral PLK1 shRNA #1 (shPLK1#1) and #2 (shPLK1#2) and then treated with TGF-β. The cells that had been invaded on the bottom layer surface were stained with 0.05% crystal violet dye, and the relative absorbance was plotted. (n = 3). e An invasion assay was performed in TGF-β-treated A549 cells after treatment with the PLK1 inhibitors volasertib and poloxin for 5 days. The absorbance was measured at a wavelength of 590 nm, and the relative absorbance was plotted. (n = 3). Data presented as mean ± SD. f A colony formation assay was performed with A549 cells depleted of PLK1, as described in the Materials and Methods. After 4 weeks, the colonies formed in agar were counted after 0.05% crystal violet staining. *p < 0.05; **p < 0.01; ***p < 0.001. (n = 3). Data presented as mean ± SD. g A colony formation assay was performed in TGF-β-treated A549 cells after treatment with the PLK1 inhibitors volasertib and poloxin. After 4 weeks, the colonies formed in agar were counted after 0.05% crystal violet staining. *p < 0.05; **p < 0.01; ***p < 0.001. (n = 3). Data presented as mean ± SD. h–i A549 cells expressing eRFP-tagged TD were treated with h shRNA targeting human PLK1 or i volasertib, and an in vitro wound-healing assay was performed 72 h after treatment. The relative migration distance was measured and plotted. *p < 0.05; **p < 0.01; ***p < 0.001. (n = 3). j–k An invasion assay was performed using A549 cells expressing eRFP-tagged TD after treatment with j shRNA for PLK1 #1 or #2 k volasertib and poloxin. The relative absorbance was measured and plotted. *p < 0.05; **p < 0.01; ***p < 0.001. (n = 3)