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. Author manuscript; available in PMC: 2022 Nov 4.
Published in final edited form as: Cancer Res Commun. 2022 May 2;2(5):277–285. doi: 10.1158/2767-9764.CRC-21-0156

FIGURE 5. Pharmacological inhibition of ALK in an ALK expressing NEPC model (MSKCC EF1) results in reduced cell viability.

FIGURE 5.

A. Western blot showing ALK expression in the prostate cancer cell lines 22rv1, DU145, PC3, LNCaP and MSKCC EF1. The molecular phenotype (AR/NE positivity) is indicated below the gel images. B. Dose-response curves of crizotinib in LNCaP, DU145, H2228 (EML4-ALK fusion), SH-SY5Y (F1117L ALK activating mutation) and MSKCC EF1 cells. C. Dose-response curves of ceritinib in LNCaP, DU145, H2228, SH-SY5Y and MSKCC EF1 cells. D. Summary table of IC50 values for crizotinib and ceritinib in LNCaP, DU145, H2228, SH-SY5Y and MSKCC EF1 cells. E. Western blots for ALK, AKT Ser471 and pan-AKT shows increased AKT phosphorylation in MSKCC EF1 cells which is inhibited by crizotinib (crizo, 5 μM) and ceritinib (ceri, 2 μM) treatment for 18 hours.