Fig. 1: High level of PDCD11 accelerates colorectal cancer progression. | Oncogenesis

Fig. 1: High level of PDCD11 accelerates colorectal cancer progression.

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

Fig. 1

A GEPIA2 was used to compare the expression level of PDCD11 in colorectal tumor (COAD + READ) and normal samples. The raw data were obtained from TCGA and the GTEx databases. FC ≥ 1.5 and q-value < 0.001 denote significant difference (*). B High-level PDCD11 indicates a high risk (HR = 1.6) of shortening the overall survival time of CRC patients (Logrank p = 0.04). Data were obtained from TCGA database and analyzed using GEPIA2. C–F All the lentivirus-transduced HCT116 cells were treated with Doxy to induce the expression of shRNAs. C The mRNA level of PDCD11 in the cells was determined by qRT-PCR (n = 3). GAPDH was used as an internal control to normalize the values. The normalized values of the cells expressing shLuc were set to 1. D Cellular level of PDCD11 protein was determined by western blotting. GAPDH was used as a loading control. E Growth curves of the cells with or without downregulation of PDCD11 (n = 3). F Cell cycle was determined by PI staining assay (n = 3). G and H Nude mice bearing lentivirus-transduced HCT116 tumors were administered with Doxy in drinking water for 12 days to downregulate the intratumor level of PDCD11. G Tumor growth curves in different groups (n = 5). H Tumor images in different groups when the 12-day course ended. C and E–G Data are shown as mean ± SD. *P < 0.05; **P < 0.01 denote significant difference.

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