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. 2017 Sep 21;8(61):103261–103273. doi: 10.18632/oncotarget.21143

Figure 5. MiR-129 suppression of Let-7b level relied on direct inhibition on estrogen receptor sustained DICER1 activity.

Figure 5

Enforced miR-129 inhibited Let-7b expression level significantly (A), so did the shRNA of estrogen receptor, and the results were significant (B). (C) After introducing miR-129 mimic into 293T cells with wild type of ESR1 or mutant type of ESR1, we identified the direct binding site between the 3’UTR of wild type-ESR1 and miR-129, and miR-129 inhibited the ESR1 level significantly. Overexpressed miR-129 suppressed the DICER1 promoter activity significantly (D). (E) The illustration of cyclin D1-ER regulated Dicer-pGL3 Luc-vector, estrogen treatment upregulated promoter activity of cyclin D1 sustained Dicer 1, and the both depletion or blocked of cyclin D1, and the mutant Dicer 1 promoter abolished the estrogen functions. (F) Little effects were detected on the luc-activity of DICER1 3’UTR when treating with estrogen (10 nM Estradiol) (Above), on the contrary, DICER1 promoter changed significantly (Below). (G) 10 nM Estradiol treatment stimulated the promoter activity of DICER1 promoter, but little effects were detected when either introducing miR-129 or inhibiting ESR1, and most importantly, no significant difference occurred between the individual regulation of miR-129 or ESR1, and the combined regulation. *p<0.05. (H) Estrogen stimulation of DICER1 activity was dependent on cyclin d1, and the inhibition of cyclin d1 abolished the activation of estrogen on DICER1 promoter.