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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: TNFAIP8 promotes AML chemoresistance by activating ERK signaling pathway through interaction with Rac1

Fig. 5

TNFAIP8 promotes cell proliferation and protects cell from apoptosis induced by chemotherapeutics in an ERK-dependent manner. a, b Representative immunoblotting of phosphorylated proteins of MAPK signaling cascades in K562, HL60 cells transduced with Flag-tagged TNFAIP8 or control vector, and corresponding resistant cell lines K562/A02 and HL60/ADR transduced with shTNFAIP8 or shNC. Cells were stimulated with doxorubicin (1 μg/mL) for 4 h. The experiment was repeated three times with similar results. c, d AML cells, K562 and HL60, transduced with Flag-tagged TNFAIP8 or control vector were treated with ERK inhibitor SCH772984 (2.5 μM). Cell proliferation was measured by CCK8 and apoptosis induced by chemotherapeutic agents was measured by flow cytometry. Data are mean ± SD values of four independent experiments calculated by two-way ANOVA followed by LSD. * P < 0.05; ** P < 0.01; *** P < 0.001

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