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. 2016 May;89(5):521–540. doi: 10.1124/mol.115.103044

Fig. 10.

Fig. 10.

Di-2-pyridylketone thiosemicarbazones (i.e., Dp44mT and DpC) markedly upregulate NDRG1 and decrease FAK/paxillin phosphorylation levels in HT29 (A) and DU145 (B). Both the NDRG1-silencing clones (sh-NDRG1) and their respective sh-Control HT29 and DU145 cells were incubated with: control medium containing 0.05% of DMSO (Control), Bp2mT (5 μM), DFO (250 μM), Dp44mT (5 μM), or DpC (5 μM) for 24 hours/37°C. Immunoblotting was then used to detect the levels of p-FAK (Tyr397, Tyr576/7, Tyr925), total FAK, p-paxillin (Tyr118), and total paxillin in response to these agents in sh-Control and sh-NDRG1 cells. Densitometry for NDRG1 and total FAK and paxillin levels are expressed relative to the loading control, β-actin, whereas the phosphorylation levels for FAK and paxillin are displayed as the ratio of the phosphorylated compared with the total proteins. Densitometry is shown as mean ± S.D. (3–5 experiments). *P < 0.05; **P < 0.01; ***P < 0.001 relative to Control cells. #P < 0.05; ##P < 0.01; ###P < 0.001 relative to cells incubated with the same treatment in the sh-Control group.