Fig. 1: TRIM39 deficiency suppresses CRC progression in vitro and in vivo. | Cell Death & Disease

Fig. 1: TRIM39 deficiency suppresses CRC progression in vitro and in vivo.

From: TRIM39 deficiency inhibits tumor progression and autophagic flux in colorectal cancer via suppressing the activity of Rab7

Fig. 1

a Kaplan–Meier survival analysis of overall survival (OS) based on TRIM39 expression in the CRC tissues from TCGA database. b Kaplan–Meier survival analysis of relapse-free survival (RFS) based on TRIM39 expression in the CRC tissues from GSE14333 database. c Analysis of TRIM39 mRNA levels in primary tumor and adjacent normal tissue in GSE90627 database. Two-way classification ANOVA. ***P < 0.001; ns no significance. d RT-PCR analysis of TRIM39 mRNA expression in HCT116, HT29, LoVo, DLD1, Caco2, SW480, and SW48 cells. e RT-PCR analysis of TRIM39 knockdown efficiency in LoVo and HCT116 cells infected with lentiviruses containing negative control shRNA (shNC) or two independent shRNAs against TRIM39. f, g The colony-formation assay (f) and soft agar colony-formation assay (g) of LoVo and HCT116 cells with TRIM39 stably knocked down. Data are shown as mean ± SD. n = 3 samples per group. One-way ANOVA. **P < 0.01; ***P < 0.001. h, i The migration assay (h) and invasion assay (i) of LoVo and HCT116 cells with TRIM39 stably knocked down. The average number of cells per field were calculated. Data are shown as mean ± SD. n = 3 samples per group, four fields per sample. One-way ANOVA. *P < 0.05; ***P < 0.001. j–l HCT116 cells (shNC, shTRIM39-1#, shTRIM39-2#) were subcutaneously injected into nude mice at a dose of 2 × 106 cells per mouse. Representative images of the xenograft tumors (j), tumor growth curves (k), and tumor weight (l) are shown. n = 5 per group; data are shown as mean ± SD for tumor weight and mean ± SEM for tumor growth. Scale bar, 2 cm. One-way ANOVA. ***P < 0.001.

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