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. 2017 Sep 4;14(5):5556–5562. doi: 10.3892/ol.2017.6886

Figure 2.

Figure 2.

UCA1 promoted the invasion and EMT of bladder cancer cells by regulating HMGB1. (A) qRT-PCR analysis of HMGB1 mRNA expression in UCA1 knockdown and overexpressing T24 and RT4 cells, respectively. (B) Confirmation of HMGB1 knockdown using siRNA in RT4 cells by qRT-PCR. (C) Transwell assays in RT4 cells with HMGB1 knockdown (HMGB1 siRNA), UCA1 overexpression (pcDNA3.1-UCA1) or HMGB1 knockdown combined with UCA1 overexpression (HMGB1 shRNA+pcDNA3.1-UCA1). (D) Western blot analysis of EMT related markers E-cadherin, N-cadherin and Vimentin expression in RT4 cells with HMGB1 knockdown (HMGB1 siRNA), UCA1 overexpression (pcDNA3.1-UCA1) or HMGB1 knockdown combined with UCA1 overexpression (HMGB1 shRNA+pcDNA3.1-UCA1). *P<0.05 vs. the control, #P<0.05 vs. pcDNA3.1-UCA1. UCA1, urothelial carcinoma associated 1; EMT, epithelial-mesenchymal transition; HMGB1, high mobility group box 1.