Fig. 3: Loss of Dsg2 in GBC cells significantly increased Src kinase activation. | Cell Death & Differentiation

Fig. 3: Loss of Dsg2 in GBC cells significantly increased Src kinase activation.

From: Loss of desmoglein-2 promotes gallbladder carcinoma progression and resistance to EGFR-targeted therapy through Src kinase activation

Fig. 3

a Phosphorylation of Src, Akt, ERK1/2, FAK, and Paxillin significantly increased in shDsg2 GBC cells. Cell lysates were analyzed by western blotting using the indicated antibodies. The pharmacological inhibition of Src kinase activity by PP2 (b) or RNA interference of cSrc mRNA by sicSrc (c) reduced Akt, ERK1/2, FAK, and Paxillin activation in shDsg2 GBC cells. Cells were treated with 10 μM PP2, 20 μM LY294002, 20 μM PD98059, or 20 μM PF-573228 for 30 min. GBC cells were transfected with 10 μM cSrc siRNA for 48 h, lysed, and subjected to western blot analysis with the indicated antibodies. d The inhibition of Src, PI3K, and MEK1/2 activity by the corresponding kinase inhibitors reduced cell proliferation (left panel). Knockdown of cSrc expression using cSrc siRNA significantly reduced GBC cell proliferation (right panel). Cell proliferation was assessed by MTT assays. *p < 0.05 compared with vehicle control (left panel) or siCtrl (right panel) cells. e Rose plots tracking the movement of five single siCtrl and sicSrc shDsg2 cells. Each color represents the track of an individual cell. f Representative images of IHC staining of Dsg2 and Src pTyr416 in clinical GBC samples. Scale bar: 50 μm.

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