Figure 3

MIR181A1HGkd causes cell cycle progression defects. (A) Proliferation curves of hMSC-hTERT20 and MIR181A1HGkd cells. (B) Cell-cycle distribution of Control and MIR181A1HG-depleted cells by FACS with PI staining (n = 2). (C) Cells were stained for BrdU incorporation and total DNA content by 7-AAD for FACS analysis. Representative cell-cycle distribution of hMSC-hTERT20, CRISPRi control and MIR181A1HG-depleted cells. (D) Representative images of BrdU immunofluorescence after 30 min incorporation. BrdU incorporation is red, while nuclei are counterstained with DAPI (blue). Scale bars represent 20 µm. (E) Quantification of BrdU incorporation by immunofluorescence (n > 700cells). **p < 0.01; ****p < 0.0001. (F) Quantification of BrdU cell cycle profiling of hMSC-hTERT20, control and MIR181A1HGkd cells. * p < 0.05; **p < 0.01; ***p < 0.005 (n = 5). (G) No significant difference was observed in phosphorylation of the mitotic marker H3S28 with MIR18A1HGkd (n > 700 cells). Data are presented as mean ± SD.