Fig 2: The effect of TR4 on viability is dependent on Bcl-2 in T24 cells. (A) EdU assay was used to evaluate the proliferation ability after knocking down the Bcl-2 expression in oeTR4-T24 cells, *p < 0.05. (B) EdU assay was used to evaluate the proliferation ability after overexpressing Bcl-2 in siTR4-T24 cells, *p < 0.05.

Fig 3: TR4 altered cell apoptosis of bladder cancer via Bcl-2: (A) The interaction network of TR4 was constructed, and the most relevant proteins involved in the cell apoptosis pathway were enclosed in a blue rectangle. (B) Bcl-2 mRNA expression was verified by qPCR after transfecting Vector, oeTR4, scr, and siTR4. (C) Bcl-2 protein expression was verified by Western blot after transfecting the Vector, oeTR4, scr, and siTR4. GAPDH was used as the internal reference. Semiquantification of Bcl-2 based on the band density from three independent experiments was shown in the right panel, *p < 0.05. (D) GEPIA was used to analyze the co-expression of TR4 and Bcl-2 in bladder cancer. Spearman = 0.25, p < 0.01. (E) TR4 motif sequence was predicted by Jaspar. (F) Bcl-2 promoter regions contain potential TR4 binding sites (TR4RE1 and TR4RE2). (G) and (H) ChIP assay results showed that TR4 binds to TR4RE2, NS: no significant, ***p < 0.001.