Fig 1: Screening tests of five compounds (including 2,4-dihydro-3H-pyrazol-3-one (DHPO) derivatives) in the expression levels of TGFß2, SMAD3, or SMAD4 in cells using Western blot. (A) Representative image; quantification of (B) TGFß2, (C) SMAD3, or (D) SMAD4 to ß-actin. Protein was separated by 12% SDS-PAGE detected by Western blot. * p < 0.05, ** p < 0.01 or *** p < 0.001 compared to CON cells. Data are the means ±SE (n = 3).
Fig 2: Effects of TSE on the mRNA or protein expression levels of TGFß2, SMAD3, SMAD4, fibronectin, or collagen I in TGFß2-induced SRA01/04 cells. (A) Representative image and (B) quantification of the ratio of target gene to ß-actin mRNA levels. The RT-PCR amplification was performed on PCR Detection System. The relative gene expression is assayed with agarose gel electrophoresis. Protein was separated by 12% SDS-PAGE detected by Western blot: (C, E) representative image, and (D, F) quantification of the target gene to ß-actin. ### p < 0.001 in comparison to control cells; * p < 0.05, ** p < 0.01 or *** p < 0.001 in comparison to TGF-ß2-induced control cells. Values are the mean ± SE (n = 3).
Fig 3: Kaplan–Meier survival curves showing overall survival in 404 patients with urothelial bladder cancer in relation to expression of TGF-ß1, Smad2 and Smad4 in cancer cells. Log Rank (Mantel–Cox) test.
Fig 4: Effects of TSE on epithelial–mesenchymal translocation of SMAD4 using confocal microscopy. The mesenchymal phenotypic marker SMAD4 (red). The nuclei were stained with DAPI (blue). Magnification, ×200.
Fig 5: Representative photomicrographs of haematoxylin–eosin stain and immunohistochemical staining to TGF-ß1, Smad2, and Smad4 in urothelial bladder cancer; first row—papillary non-invasive low grade tumor (pTa); second row—superficially invasive low grade tumor (pT1); third row—superficially invasive high-grade tumor (pT1); fourth row—muscle-invasive urothelial bladder cancer (pT2). Original magnification ×400.
Supplier Page from Abcam for Anti-Smad4 antibody