Figure 5

c-RAF–PDE8A disruption attenuates PANC1 adherence and migration. (A) Cell area (µm²) in untreated vs. DMSO vs. DRx-170 (1 μM) treated (24 h) PANC1 cells (n ≥ 60 cells per group, N = 3, scale bar = 10 µm). (B)(i) RTCA (xCELLigence) of PANC1 cell adherence following 8 h treatment with vehicle (1% DMSO), DRx-150 (0.14 µM) or DRx-170 (0.035–1.4 µM). (B)(ii) Representative bar chart of relative PANC1 (slope of curve) adherence (N = 3). ns, not significant; #, P < 0.05 vs. DRx-150 and Vehicle. (C)(i) PANC1 cell migration analysis (in vitro wound healing, scale bar = 500 µm) following 24 treatment with vehicle (1% DMSO), DRx-150 (1 µM), DRx-170 (0.1–10 µM). Blue outline highlights ‘wound’ at time point 0 h and 24 h. (C)(ii) Representative bar chart of relative PANC1 migration (i.e., relative % wound gap closure) (N ≥ 3). (D) In vitro cell viability (endpoint) assessment of non-cancerous human cell lines HEK293, IMR-90 following 72 treatment with DRx-170 (0.001–10 µM, N ≥ 3). Horizontal line represents vehicle 100% viability control MEAN ± SEM, ns, not significant; *P < 0.05.