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. 2017 Mar 23;8(20):33475–33486. doi: 10.18632/oncotarget.16509

Figure 4. miR-217 suppresses DNMT1 expression during HSF senescence.

Figure 4

Abbreviations: c-i: control inhibitors; miR-i: miR-217 inhibitors; c-sh: control shRNA; DNMT1-sh: DNMT1 shRNA lentivirus; c-m: control mimics; miR-m: miR-217 mimics; con: control adenovirus; DNMT1: DNMT1 adenovirus. (A) DNMT1 expression was detected by western blot analysis. The DNMT1 shRNA lentivirus partially reversed DNMT1 upregulation caused by the miR-217 inhibitors (*p < 0.05). (B) DNMT1 expression was detected by western blotting. The DNMT1 adenovirus partially reversed DNMT1 downregulation caused by the miR-217 mimics (*p < 0.05). (C) HSF growth rates were determined by performing MTT assays. The DNMT1-shRNA lentivirus partially reversed the increased proliferation rate caused by the miR-217 inhibitors (n = 3 for each time point, *p < 0.05). (D) HSF growth rates were detected by performing MTT assays. The DNMT1 adenovirus could partially reverse the decreased proliferation rate caused by the miR-217 mimics (n = 3 at each time point, *p < 0.05). (E) HSF senescence was measured by determining the percentage of SA-β-gal-positive cells. Transduction with the DNMT1 shRNA lentivirus partially reversed the decreased SA-β-gal-positive ratio caused by the miR-217 inhibitors (*p < 0.05; left panel). Quantification of the SA-β-gal-positive rate is shown in the right panel (n = 3, *p < 0.05). (F) HSF senescence was evaluated by determining the number of SA-β-gal-positive cells. The DNMT1 adenovirus did significantly inhibit the increased SA-β-gal-positive ratio caused by the miR-217 mimics (*p < 0.05; left panel). Quantification of the SA-β-gal-positive ratio is shown in the right panel (n = 3, *p < 0.05).