Fig. 2
CircMYH9 promoted cell growth in CRC cells. A-B CCK-8 and colony formation assays detected cell viability of the circMYH9-depleted HCT116 cells and control HCT116 cells. C-D CCK-8 and colony formation assays detected cell viability of the circMYH9-overexpressing LoVo cells and control LoVo cells. E Flow cytometry was used to assess the cell cycle of the circMYH9-depleted HCT116 cells and control HCT116 cells. F Cell cycle proteins (CDK1, Cyclin D1, CDK6, Cyclin E2) were assessed by immunoblotting in the circMYH9-depleted HCT116 cells and control HCT116 cells. G Flow cytometry was used to assess the cell cycle of circMYH9-overexpressing LoVo cells and control LoVo cells. H Cell cycle proteins (CDK1, Cyclin D1, CDK6, Cyclin E2) were assessed by immunoblotting in the circMYH9-overexpressing LoVo cells and control LoVo cells. I Image of xenograft tumours in BALB/c nude mice subcutaneously injected with the circMYH9-depleted and their respective parental cells (5 × 106 cells per mouse). The mice were sacrificed after 3 weeks, and subcutaneous xenograft tumours were collected. J Tumour growth curves represented as the tumour volume of the circMYH9-depleted HCT116 cells and their respective parental cells in xenograft models at the indicated time intervals (n = 5 per group). K Tumour weights of the two groups were measured after sacrifice (n = 5 per group). L-N Image of xenograft tumours, tumour growth curves and tumour weights in BALB/c nude mice subcutaneously injected with the circMYH9-overexpressing and their respective parental cells (5 × 106 cells per mouse). O-P IHC analysis of Ki-67 expression in sections obtained from xenograft models. Data are shown as the mean ± SD from three independent experiments (*, P < 0.05; **, P < 0.01)