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. 2017 Nov 13;12(3):236–246. doi: 10.1080/19336918.2017.1365992

Figure 4.

Figure 4.

Effect of over-expression of TGFBR3 on migration, EMT and NF-κB activity in CAL-27 cells. CAL-27 cells were transfected for 24 h with 1 µg/ml of plasmid encoding TGFBR3. EV represents empty vector (1 µg/ml of pc-DNA3.1 plasmid)-transfected CAL-27 cells. (A) TGFBR3 expression was determined by western blot analysis and the average band densities from three independent experiments are shown. (B) Scale bars, 10 µm. TGFBR3 overexpression inhibits migration in CAL-27 cells. Following plasmid transfection, cells were subjected to Transwell migration. (C, D) The EMT-related markers, E-cadherin (E-cad) and Vimentin (Vim) were up-regulated and down-regulated after TGFBR3 over-expression for 24 h, respectively. (E) Transient increases in TGFBR3 expression decreased p-p65 expression. (F) Transient increases in TGFBR3 expression resulted in concomitant increases in IκBα expression. (G) TGFBR3 interacts with β-arrestin 2; β-arrestin 2 interacts with IκBα. (J) CAL-27 cells transiently transfected with β-arrestin 2 siRNA. (H) TGFBR3 overexpression decreased p-p65 expression, and co-transfection of TGFBR3 and β-arrestin 2 siRNA resulted in an increase in phosphorylation of p65. Data are presented as mean ± standard deviation following three independent experiments. *p < 0.05 vs. control; # p < 0.05 vs. TGFBR3.