Fig. 2: PDCD11 accelerates colorectal cancer cell growth by modulation of p53-CDK1 and CDC25C-CDK1 axes. | Oncogenesis

Fig. 2: PDCD11 accelerates colorectal cancer cell growth by modulation of p53-CDK1 and CDC25C-CDK1 axes.

From: Programmed cell death 11 modulates but not entirely relies on p53-HDM2 loop to facilitate G2/M transition in colorectal cancer cells

Fig. 2

All the lentivirus-transduced cells were treated with Doxy to induce the expression of shRNAs. A The mRNA levels of PDCD11, p53, HDM2, p21, CDC25C, and CDK1 in HCT116 cells were determined by qRT-PCR (n = 3). GAPDH was used as an internal control to normalize the values. The normalized values of HCT116p53+/+ cells expressing shLuc were set to 1. B The levels of PDCD11, p53, HDM2, p21, CDC25C, p-CDK1-Y15, and CDK1 proteins in the cells were determined by western blotting. GAPDH was used as a loading control. p-CDK1/CDK1 ratio indicates relative phosphorylation rate of CDK1 and the values of the cells expressing shLuc were set to 1 for normalization. C, D Western blot analyses were performed to investigate the levels of CDC25C, CDK1, and p-CDK1-Y15 proteins in PDCD11-downreguatled HCT116 cells transfected with pcDNA3-Luc, pcDNA3-CDC25C, or pcDNA3-CDK1. GAPDH was used as a loading control. p-CDK1/CDK1 ratio indicates relative phosphorylation rate of CDK1 and the values of the cells expressing Luc were set to 1 for normalization. E, F Cell growth curves of PDCD11-downregulated HCT116 cells transfected with pcDNA3 plasmids (n = 3). A, E, and F Data are shown as mean ± SD. *P < 0.05; **P < 0.01 denote significant difference.

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