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. 2017 Jun 18;11(9):1189–1207. doi: 10.1002/1878-0261.12088

Figure 5.

Figure 5

TrkAi efficiently decreases TrkA tyrosine kinase activity and the phosphorylation of survival‐promoting proteins in NPM‐ALK + T‐cell lymphoma cells. (A) Treatment of SR‐786, SU‐DHL‐1, and SUP‐M2 cells with the TrkAi induced a significant decrease in TrkA tyrosine kinase activity. Results shown are means ± SE of three independent experiments (*P < 0.0001 vs. vehicle‐treated cells). (B) WB shows that at 48 h TrkAi induced downregulation of pTrkA levels in SR‐786 cells. The decrease in pTrkA was associated with a significant decrease in pNPM‐ALK, pIGF‐IR, pAKT, and pSTAT3. These effects were more pronounced at the 30 μm concentration. Changes were not detected in the total protein levels. Moreover, treatment with TrkAi decreased the levels of caspase 3, BCL‐2, and BCL‐XL, attesting to apoptosis occurrence. β‐Actin was used as the loading control. MW: TrkA and pTrkA, 140 kDa; NPM‐ALK and pNPM‐ALK, 80 kDa; IGF‐IR and pIGF‐IR, 95 kDa; AKT and pAKT, 60 kDa; STAT3 and pSTAT3, 86 kDa; caspase 3, 32 kDa; BCL‐2, 26 kDa; BCL‐XL, 30 kDa.