Fig. 6

TRIM37 promotes RCC tumorigenesis and metastatic potential in xenograft models. A, TRIM37 overexpression significantly promoted the tumor volume of subcutaneous model than NC group. B-C, TRIM37 overexpression significantly improved the tumor size and weight than NC group. D, The mice weights gradually improved in both NC and TRIM37 overexpression group. There is no statistical difference between two groups. E, compared to NC group, tumors in TRIM37-overexpression group displayed significantly enhancive Ki67 and PCNA expression, as well as upregulated ub-H2A and TGF-β1 levels. F, Overexpression of TRIM37 accelerated more RCC cells to metastasize to pulmonary foci compared with control group, accompanied with higher fluorescence signal. G, More pulmonary foci were visibly observed in TRIM37 overexpression group. H, Using clinical RCC samples, TRIM37, TGF-β1 and EMT markers (N-cadherin and Vimentin) were correlatively upregulated in metastatic sites than primary lesions. I, Immunoblot assay demonstrated higher TRIM37, TGF-β1 and EMT markers in metastatic lesions than primary lesions. J, Model depicting the mechanism by which TRIM37 orchestrates RCC progression via TGF-β1/Smad2/3 signaling under a histone H2A ubiquitination-dependent manner