Fig. 6: NCK synergizes with MEK inhibitors in KRAS-mutant PDAC cells by stimulating apoptosis. | Cell Death & Disease

Fig. 6: NCK synergizes with MEK inhibitors in KRAS-mutant PDAC cells by stimulating apoptosis.

From: Concurrent inhibition of pBADS99 synergistically improves MEK inhibitor efficacy in KRASG12D-mutant pancreatic ductal adenocarcinoma

Fig. 6

A Heatmap plot depicts quantification of crystal violet staining of foci of SW1990 and Panc-1 cells after exposure to vehicle (V), NCK (N), MEK inhibitors (T, S or B), or NCK + MEK inhibitors (N + T, N + S or N + B) for 9 days. Data represent ratio of cell viability relative to the vehicle (mean, n = 3). *P < 0.05, **P < 0.01, and ***P < 0.001. B Microscopic visualization of Calcein-AM (green) stained colonies (live) and BOBO-3 Iodide (red) stained cell debris (dead) generated by SW1990 and Panc-1 cells cultured in 3D Matrigel after exposure to vehicle (V), NCK (N), MEK inhibitors (T, S or B), or NCK + MEK inhibitors (N + T, N + S or N + B) for 12 days. Scale bars, 100 μm. C CASPASE 3/7 activities were evaluated in SW1990 and Panc-1 cells after the respective treatments for 72 h using the Biovision Caspase 3/7 DEVD Assay Kit. Data represent means ± SD (n = 3). *P < 0.05, **P < 0.01, and ***P < 0.001. D. Western blot analysis was used to assess the level of BAD and apoptotic proteins in SW1990 and Panc-1 after treatment with vehicle (V), NCK (N), MEK inhibitors (T, S or B), and their combinations (N + T, N + S or N + B) for 72 h. β-ACTIN was used as input control. The sizes of detected protein bands in kDa are shown on the left.

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