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. 2018 Apr 10;9(27):18949–18969. doi: 10.18632/oncotarget.24855

Figure 3. HK1 knockdown causes a typical EMT change and accelerates tumor cell motility.

Figure 3

(A) Fluorescence imaging of stress fibres in HK1-silenced cells. Cells as indicated were fixed and then stained with Alexa Fluor 488-conjugated phalloidin. (B) Western blotting of E-cadherin, vimentin and α-SMA in HK1-inhibited cells. Total protein extracts isolated from cells as indicated were blotted with antibodies specific for proteins as labelled. The β-actin level serves as the loading control for total proteins. (C and D) Immunofluorescent staining of E-cadherin and vimentin in HK1-knocked down cells. Cells as indicated were stained with antibody specific for E-cadherin or vimentin; nuclei were counterstained with DAPI. (E) Wound healing migration assay of HK1-inhibited cells. Cells as indicated were cultured until confluent, then the wound healing migration assay carried out; the wounds were imaged after incubation for various time periods as labelled. (F) Boyden chamber migration assay of HK1-knocked down cells. Cells as indicated were loaded into Boyden chambers, then migrated chemotactically for 6 h. The cells that migrated were stained, imaged and enumerated. (G) Matrigel invasion assay of HK1-silenced cells. Cells as indicated were seeded in invasion chambers, the invaded and penetrated chemotactically for 8 h. The cells that invaded were stained, imaged and enumerated. The plotted data are averaged from three independent experiments and the bars represent mean ± SD.