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. 2012 Nov 8;2:785. doi: 10.1038/srep00785

Figure 2. CS knockdown induces morphological changes with EMT features in human cervical cancer cells.

Figure 2

(A) Colony morphology of cells stably transfected with the pshCS1 construct. HeLa and SiHa cells were first transfected with pshCS1 and then screened for drug resistance. Several stable drug-resistant clones were selected and imaged. (B) Immunofluorescence staining of CS expression in pshCS1-transfected cells. Cells displaying either epithelial or fibroblast-like morphology were immunostained with antibody for CS. (C) Western blotting of CS expression in pshCS1-transfected cells. Total proteins isolated from cells displaying either epithelial or fibroblast-like morphology were blotted with antibodies for CS and β-actin. (D) CS activity assay of pshCS1-transfected cells. Total proteins isolated from cells displaying either epithelial or fibroblast-like morphology were subjected to CS activity assay. (E) Morphological imaging of CS knockdown cells. Four selected CS knockdown clones as indicated were photographed. (F) Fluorescence imaging of stress fibers in CS knockdown cells. Indicated cells were stained with Alexa Fluor 488-conjugated phalloidin and DAPI. (G) Western blotting of epithelium- or mesenchyme-specific proteins in CS knockdown cells. Total proteins isolated from indicated cells were blotted with antibodies as labeled. (H and I) Immunofluorescence staining of E-cadherin and Vimentin in CS knockdown cells. Indicated cells were immunostained with antibody for E-cadherin or Vimentin, and DAPI. The amount of β-actin serves as loading control. The plotted data were averaged from three independent experiments and the bars represent mean ± SD.