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. 2015 Sep 9;10(9):e0136893. doi: 10.1371/journal.pone.0136893

Fig 2. Acute cisplatin induces functional activation of the EGFR thereby activating downstream signaling pathways JAK2 and AKT.

Fig 2

A) Representative western blots of pEGFR, Total EGFR and GAPDH of OVCA 433 cells-/+ 10 μM cisplatin for 1 hour in the presence and absence of the EGFR specific inhibitor AG1478 (2 μM, for 24 hour pre-incubation). B) Representative western blots for pJAK2 (tyr1007/1008), total JAK2, pAKT (ser473), total AKT and GAPDH. OVCA 433 cells-/+ 10 μM cisplatin for 1–4 hours and in presence of AG1478. The data generated for the following graphs represent at least 4 independent experiments i.e. ~4 different treatment/collection groups and ~4 different immunoblots. C) Ratio of JAK2 activation (pJAK2/total JAK2) data obtained after 10 μM cisplatin treatment for 1–4 hours and in the presence of AG1478, n = 4–6. Significant increases from control samples observed at 4 hours of cisplatin treatment. AG1478 pre-incubation for 24 hours blunted basal levels of activated JAK2 as well as cisplatin induced increases in JAK2 activation at 4 hours (AG+4). D) Ratio of AKT activation (pAKT/total AKT) data obtained after 10 μM cisplatin treatment for 1–4 hours and in the presence of AG1478, n = 4–7. Significant increases from control samples observed at 4 hours of cisplatin treatment. AG1478 pre-incubation for 24 hours blunted cisplatin induced increases in AKT activation at 4 hours (AG+4). One-way ANOVA revealed a significant effect of drug treatment and following Dunnet’s post hoc test significant differences from controls are indicated by *p<0.05, **p<0.01.