Fig. 6: CDK1 rescued a decrease in cell proliferation and growth induced by knockdown of RBM7.

a Western blot and b, c RT-qPCR were used to verify the efficiency of CDK1 overexpression and CDK1 mutant overexpression in the knockdown of RBM7 or control in SUM-1315 and MCF-7 cells. The relative quantification was calculated by the 2^−ΔΔCt method and normalized based on β-actin (*P < 0.05). The fold change of CDK1 protein was shown below each lane. The intensity of the bands was determined using densitometric analysis. Cell proliferation assays of RBM7 knockdown or control in SUM-1315 (e) and MCF-7 (f) cells after cotransfection with CDK1 or CDK1 mutant by CCK-8. Data represented as mean ± SD (*P < 0.05). Colony formation assays of RBM7 knockdown or control in SUM-1315 (h) and MCF-7 (i) cells after co-transfection with CDK1 or CDK1 mutant. Representative photographs (upper) and quantification (lower) were shown (g–i). SCR-MSA represented the control cells; Sh-1-MSA represented RBM7 knockdown cells; Sh-1-CDK1 represented RBM7 knockdown + CDK1 overexpression cells; Sh-1-CDK1-MUT represented RBM7 knockdown + CDK1-MUT overexpression cells. d SUM-1315 cells were injected subcutaneously into the left breast of nude mice. The tumor tissues were stained with H&E. Scale bars indicated 20 μm. j The photograph represented the tumor tissues in RBM7 knockdown + CDK1 overexpression (Sh-1-CDK1), RBM7 knockdown + CDK1-MUT overexpression (Sh-1-CDK1-MUT), RBM7 knockdown (Sh-1-MSA) and the control group (SCR-MSA). k CDK1 expression of the tumor tissues was elevated by Western blot analysis. The fold change of CDK1 protein was shown below each lane. The intensity of the bands was determined using densitometric analysis. l CDK1 reversed the tumor weights decrease induced by RBM7 in vivo. The tumor weights were got on day 24. m The tumor volumes growth curves were monitored and recorded every 4 days. The data were represented as mean ± SD (*P < 0.05).