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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

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

Fig. 2

ELF1 promotes human TNFAIP8 gene transcription in AML. a ELF1 expression in AML patient samples (n = 173, red) and control BM samples (n = 70, grey) from TCGA database. b Correlation of TNFAIP8 and ELF1 expression (Log2 transformed values; Pearson correlation, R) in AML patients from TCGA database. c TNFAIP8 and ELF1 expression in K562 and HL60 cells infected with lentivirus harboring ELF1 (ELF1) or negative control (Mock) by RT-qPCR. Data are mean ± SD values of three independent experiments. * P < 0.05; ** P < 0.01; *** P < 0.001. d The putative promoter of the TNFAIP8 was cloned upstream of firefly luciferase to yield plasmid TNFAIP8-Prom. TNFAIP8-Prom or empty pGL4.10 vector was transfected into 293 T cells. Dual-luciferase activity was measured 48 h after transfection by a luminometer. Luciferase activity was normalized for Renilla luciferase. Results are represented as mean ± SD and calculated as fold induction relative to cells transfected with TNFAIP8-Prom plasmid. e 293 T cells were transfected with the indicated luciferase reporter plasmids, together with ELF1 expression plasmid. Results are represented as mean ± SD and calculated as fold induction relative to cells transfected with TNFAIP8-Prom plasmid and control blank vector of ELF1. f, g ChIP analysis of ELF1 binding to TNFAIP8 promoter region. Input served as a positive control and IgG IP was used as a negative control for ChIP. The fold enrichment values were normalized to the negative control IgG. Data are mean ± SD values of three independent experiments calculated by Mann-Whitney U test or unpaired Student t-test. * P < 0.05; ** P < 0.01; *** P < 0.001 versus the IgG group, ns = not significant

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