Figure 4
Figure 4. The STAT3 targeted gene, Pim1, is significantly lost in ATL tumors established from mice. (A) Real-time PCR analysis in ED-40515(–) pTRIPZ or miR-124a TET-On tumors. Each line represents the expression of the target gene (-ΔCt) between pTRIPZ and miR-124a in the corresponding mice. P values are calculated using a 2-tailed Student t test between the -ΔCt values for pTRIPZ vs miR-124a (n = 10). (B) Correlation graph plotting Pim1 expression (-ΔCt; y-axis) vs miR-124a expression (-ΔCt; x-axis) in ED-40515(–) tumors. The Spearman correlation coefficient is indicated along with corresponding P value. (C-D) Pim1 expression is decreased by immunohistochemistry staining (C) or western blot (D) in ED-40515(–) pTRIPZ or miR-124a TET-On tumors. Images were taken at room temperature on a Nikon Eclipse 80i microscope (Nikon Instruments, Inc.; Melville, NY) and a Nikon DSFI1 camera, with a 40× objective lens. Pim1 (E) and Pim1 target genes SOCS3, p-Bcl2 (Ser70), p-4EBP1 (Thr37/46), and p-p70S6K (Thr389) (F) were analyzed by western blot in miR-124a TET-On, ED-40515(–), and Tl-Om1 induced with 2 µg/mL Dox for 72 hours. (G) Illustration of the miR-124a binding sites in the 3′-UTR of Pim1. Pim1 UTR luciferase (H) or Pim1 western blot (I) was performed in 293T cells. pCDNA and miR-124a/pCDNA (left) or pCDNA and miR-33a/pCDNA or miR-214/pCDNA (right) were transfected into 293T cells, along with the RL-TK plasmid. Forty-eight hours after transfection, cell lysates were measured for firefly (Pim1 UTR) and renilla (RL-TK, internal control) activity. All luciferase was performed at least twice. (J) Exogenous STAT3 expression rescues miR-124a–mediated inhibition of Pim1. pCDNA (control) or STAT3-HA–tagged lines were established under puromycin selection in 293T cells, transefected with miR-124a or negative oligos, and analyzed several days later for Pim1 expression. Stable STAT3 expression was detected by HA antibodies.

The STAT3 targeted gene, Pim1, is significantly lost in ATL tumors established from mice. (A) Real-time PCR analysis in ED-40515(–) pTRIPZ or miR-124a TET-On tumors. Each line represents the expression of the target gene (-ΔCt) between pTRIPZ and miR-124a in the corresponding mice. P values are calculated using a 2-tailed Student t test between the -ΔCt values for pTRIPZ vs miR-124a (n = 10). (B) Correlation graph plotting Pim1 expression (-ΔCt; y-axis) vs miR-124a expression (-ΔCt; x-axis) in ED-40515(–) tumors. The Spearman correlation coefficient is indicated along with corresponding P value. (C-D) Pim1 expression is decreased by immunohistochemistry staining (C) or western blot (D) in ED-40515(–) pTRIPZ or miR-124a TET-On tumors. Images were taken at room temperature on a Nikon Eclipse 80i microscope (Nikon Instruments, Inc.; Melville, NY) and a Nikon DSFI1 camera, with a 40× objective lens. Pim1 (E) and Pim1 target genes SOCS3, p-Bcl2 (Ser70), p-4EBP1 (Thr37/46), and p-p70S6K (Thr389) (F) were analyzed by western blot in miR-124a TET-On, ED-40515(–), and Tl-Om1 induced with 2 µg/mL Dox for 72 hours. (G) Illustration of the miR-124a binding sites in the 3′-UTR of Pim1. Pim1 UTR luciferase (H) or Pim1 western blot (I) was performed in 293T cells. pCDNA and miR-124a/pCDNA (left) or pCDNA and miR-33a/pCDNA or miR-214/pCDNA (right) were transfected into 293T cells, along with the RL-TK plasmid. Forty-eight hours after transfection, cell lysates were measured for firefly (Pim1 UTR) and renilla (RL-TK, internal control) activity. All luciferase was performed at least twice. (J) Exogenous STAT3 expression rescues miR-124a–mediated inhibition of Pim1. pCDNA (control) or STAT3-HA–tagged lines were established under puromycin selection in 293T cells, transefected with miR-124a or negative oligos, and analyzed several days later for Pim1 expression. Stable STAT3 expression was detected by HA antibodies.

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