Fig. 3: Downregulation of PDCD11 sensitizes cells to DNA damage stress-induced G2/M arrest and apoptosis. | Oncogenesis

Fig. 3: Downregulation of PDCD11 sensitizes cells to DNA damage stress-induced G2/M arrest and apoptosis.

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

Fig. 3

All the lentivirus-transduced HCT116 cells were treated with Doxy to induce expression of shRNAs. Prior to be harvested, the cells were untreated or treated with 1 μM Adr for 24 h. A, B Cell cycle was determined by PI staining assay (n = 3). Sub-G1 indicates the apoptotic cell population. C The levels of PDCD11, Caspase-3 (full-length and cleaved p17), p53, HDM2, p14ARF, 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. D A model showing the role of PDCD11 in response to DNA damage stress (DDS). In the absence of p53, PDCD11 relaxes the G2/M checkpoint when cells were arrested in G2 phase by DDS. In the presence of p53, PDCD11 turns to resist DDS-induced apoptosis of G2-phase cells.

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