Fig. 3

TRIM37 promotion of RCC progression and EMT depends on canonic TGF-β1/Smad signal. A-B, TRIM37 ablation inhibited TGF-β1, Smad2, Smad3, ZEB-1 and Snail activity in Caki-1 and Caki-2 cells, while overexpression enhanced their expression in 786-O and ACHN cells. C, Rh TGF-β1 stimulator reversed TGF-β1/Smad2/3 signaling inhibited by TRIM37 silencing. D, Rh TGF-β1 stimulator reversed EMT plasticity phenotypes (N-cadherin and Vimentin increased, Claudin-1 decreased) inhibited by TRIM37 silencing. E, TRIM37 knockdown inhibited Matrigel based invasion, and Rh TGF-β1 stimulator restored the invasive potential suppressed by TRIM37 downregulation in Caki-1 and Caki-2 cells. F, Immunoprecipitation assay using TRIM37 antibody indicated that TRIM37 could not directly interact with TGF-β1 in Caki-1 and Caki-2. G, Altered frequencies of TRIM37 and TGF-β1 signaling gene in TCGA datasets, including TRIM37 (5%), TGF-β1 (4%), Smad2 (7%) and Smad3 (4%). H, Correlative analysis declared that TRIM37 expression positively correlated with TGF-β1 expression in TCGA datasets, NMU_RCC cohort1 and CCLE RCC cell lines analysis. I, GSE11151 datasets showed TGF-β1 expression was upregulated in tumors than normal tissues. J, Overall survival role of TGF-β1 in TCGA datasets. High TGF-β1 expression predicted shorter overall survival time in TCGA RCC cohort