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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

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

Fig. 7

TNFAIP8 suppression decelerates AML progression in vivo. a Schematic design of murine AML models. Murine AML cell line C1498 cells was transduced with Tnfaip8 shRNA (shTNFAIP8) or nonsilencing scrambled control (shNC). C57BL/6 mice were injected with 2 × 105 C1498 cells (shTNFAIP8 or shNC) through tail vein. b C1498 cells (shTNFAIP8 or shNC) were sorted for GFP positivity followed by RT-qPCR and western blots. c C57BL/6 mice from shTNFAIP8 and shNC group (n = 5 in each group) were euthanized to evaluate tumor burden at day 24. Representative flow cytometry plots and summary data of GFP-positive cells rates in blood, bone marrow (BM), liver and spleen. d Representative examples and summary weight data of livers and spleens derived from two groups of leukemic mice. e Representative Hematoxylin and eosin (H&E) images (original magnification 50× and 400×) from two groups showing different infiltration levels of tumor in blood, bone marrow (BM), liver and spleen. f Representative immunohistochemical (IHC) images (original magnification 200×) of BM specimens from two groups showing a difference in TNFAIP8 and p-ERK expression. Data are mean ± SD values. * P < 0.05; ** P < 0.01; *** P < 0.001. g For survival analysis, C57BL-6 mice were engrafted with C1498 cells transduced with TNFAIP8 shRNA or nonsilencing scrambled control (n = 5 in each group) and monitored until ethical euthanasia according to signs of morbidity. Survival was plotted by using the Kaplan-Meier method

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