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. Author manuscript; available in PMC: 2011 Dec 10.
Published in final edited form as: Mol Cell. 2010 Dec 10;40(5):762–773. doi: 10.1016/j.molcel.2010.11.038

Figure 7. miR-17-92 targets multiple components of the TGFβ-pathway.

Figure 7

(A) The relative mRNA expression of TGFβ-responsive genes in tetracycline treated (+TET) and untreated SHEP-TR-miR-17-92 cells (+TET) (mean ± SEM). (B) Significant negative correlation between TGFBR2 mRNA expression and miR-17-92 expression and SMAD2 mRNA expression and miR-17-92 expression in primary neuroblastoma tumors. Spearman’s rank rho-values and p-values are listed. (C)(D) The relative mRNA expression (mean ± SEM) of a representative set of genes responsive to TGFβ (C) and genes not or (indirectly) responsive to TGFβ (D) in SHEP-TR-miR-17-92 cells that were either untreated, treated with TGFβ-inhibitor or treated with TGFβ-inhibitor followed by miR-17-92 activation with tetracycline (TET) for 24h. (C) Genes respond to TGFβ-inhibitor treatment (t-test, p < 0.05, indicated by *) and show an additional decrease in expression upon combined TGFβ-inhibitor treatment and miR-17-92 activation (t-test, p < 0.001, indicated by *). (D) Genes only respond to mR-17-92 treatment (t-test, p < 0.001, indicated by **). (E) Relative 3’UTR luciferase reporter activity for TGFBR2, SMAD2 and SMAD4, measured in DLD1DICERhypo cells (mean ± SEM). Plasmids with a wild type seed site for the active miRNA were introduced in DLD1DICERhypo cells in combination with a pre-miR negative control (NC) or miR-17-92 pre-miR. Luciferase activity is decreased significantly in the presence of the active miRNA (*) (t-test, p < 0.01) and increases significantly when the seed for the active miRNA is mutated (MUT) (t-test, p < 0.01).