Profiling RTK phosphorylation depicts sunitinib as a potential drug for RTK inhibition in neuroblastoma.

<p>(<b>A</b>) Representative nitrocellulose membranes showing the RTKs activation profile of SH-SY5Y, SK-N-BE(2) and IMR-32 NB cell lines before and after treatment with 1 µM dose of sunitinib for 72 h. (<b>B</b>) Sunitinib effect on its principal targets represented graphically as fold of inhibition respect to control. (<b>C</b>) Effect of sunitinib on the phosphorylation of other RTKs (fold change vs. control). (<b>D</b>) Effect of 72 h treatment with sunitinib on SH-SY5Y, SK N BE(2), SK-N-AS and IMR-32 NB cell lines analyzed by Western blot with pSer⁴⁷³Akt, Akt, pThr²⁰²/Thr²⁰⁴ Erk1/2 and Erk1/2 antibodies. β-actin was used as a loading control. (<b>E</b>) Sunitinib induces the phosphorylation of Erk1/2 from 24 hours of sunitinib treatment. All experiments were performed in triplicate.