Figure 7
Figure 7. miR-193a inhibits leukemic growth in vivo. (A) Diagram illustrating the experimental design of the mice xenograft experiment. (B) Tumor volumes measured at the indicated days during the experiment. WT (n = 3), scramble (n = 6), and synthetic miR-193a (n = 6). (C) Tumor weight averages and (D) photographs of 2 mice between scramble and synthetic miR-193a–treated mice groups at the end of the experiment (day 14; P = .001). Bars represent SD. (E) Ectopic miR-193a expression significantly inhibits tumor growth in mice engrafted with SKNO-1 cells. (F) Relative quantification of indicated gene expression in xenografts injected with synthetic miR-193a or scramble. (G) Immunoblot analysis demonstrated the down-regulation of AML1/ETO, KIT and indicated downstream effectors in xenografts injected with synthetic miR-193a or scramble. (H) Schematic model for the epigenetic silencing of miR-193a and PTEN genes by AML1/ETO and the interplay among AML1/ETO corepressor complex, miR-193a, PTEN, KIT, and CCND1 in myeloid differentiation.

miR-193a inhibits leukemic growth in vivo. (A) Diagram illustrating the experimental design of the mice xenograft experiment. (B) Tumor volumes measured at the indicated days during the experiment. WT (n = 3), scramble (n = 6), and synthetic miR-193a (n = 6). (C) Tumor weight averages and (D) photographs of 2 mice between scramble and synthetic miR-193a–treated mice groups at the end of the experiment (day 14; P = .001). Bars represent SD. (E) Ectopic miR-193a expression significantly inhibits tumor growth in mice engrafted with SKNO-1 cells. (F) Relative quantification of indicated gene expression in xenografts injected with synthetic miR-193a or scramble. (G) Immunoblot analysis demonstrated the down-regulation of AML1/ETO, KIT and indicated downstream effectors in xenografts injected with synthetic miR-193a or scramble. (H) Schematic model for the epigenetic silencing of miR-193a and PTEN genes by AML1/ETO and the interplay among AML1/ETO corepressor complex, miR-193a, PTEN, KIT, and CCND1 in myeloid differentiation.

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