Figure 3. Activation of cMet is differentially regulated in epithelial and mesenchymal non–small‐cell lung cancer (NSCLC) cell lines following Plk1 inhibition and knockdown.

• A
  Three pairs of TGF‐β–treated isogenic NSCLC cell lines (H1975, HCC4006, and HCC366) and two mesenchymal NSCLC cell lines (Calu6 and H1792) were incubated with 50 nM volasertib for 24 h, lysed, and subjected to reverse phase protein array analysis. Experiments were done in triplicate.
• B
  Thirty‐three proteins were differentially regulated between epithelial and mesenchymal NSCLC cell lines after treatment with volasertib, including those involved in the cMet/FAK/Src signaling axis (blue text) and those involved in the PI3K/Akt signaling axis (orange text).
• C
  The same cell lines treated identically were subjected to immunoblotting for the indicated proteins (upper) with densitometric quantification normalized with β‐actin (lower).
• D
  Epithelial (red text) and mesenchymal (blue text) NSCLC cell lines transfected with 10 nM siRNA as indicated for 48 h and subjected to Western blotting with the indicated antibodies (upper) with densitometric quantification normalized with β‐actin (lower). NT, non‐targeting control.
• E
  H1975 and Calu6 cells were treated with indicated inhibitors for 4 h or 24 h. Cells were then harvested, and lysates were immunoblotted for the indicated proteins.

Data information: Data are means ± standard error of the mean from three independent experiments. Significant differences using two‐sided Student's t‐test are indicated by *P < 0.05.Source data are available online for this figure.