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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: FAM167A is a key molecule to induce BCR-ABL-independent TKI resistance in CML via noncanonical NF-κB signaling activation

Fig. 5

FAM167A contributes to BCR-ABL-independent TKI resistance in vitro. A Schematic diagram depicting inhibition of the FAM167A-induced noncanonical NF-κB pathway. B Viability of K562R cells transfected with a plasmid encoding NIK-DN after treatment with imatinib or nilotinib (Nilo) for 3 days. C Viability analysis of K562R cells after treatment with 2 μg/ml of anti-FAM167A neutralizing antibody or an isotype control for 3 days in the presence of imatinib or nilotinib. D The apoptotic population of K562R cells after treatment with 2 μg/ml of anti-FAM167A neutralizing antibody or an isotype control for 3 days in the presence of imatinib or nilotinib. Data are representative of three (B-D) independent experiments (error bars, s.d. of triplicate (B-D) samples). Unpaired two-tailed t-test; *P < 0.05, **P < 0.01, ***P < 0.001

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