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. 2018 Jan 18;9(2):27. doi: 10.1038/s41419-017-0189-y

Fig. 4. Overexpression of PCDHGA9 inhibited the EMT process induced by TGF-β.

Fig. 4

a, c PCDHGA9 was downregulated in artificial EMT models induced by TGF-β in GC cells. Up or downregulated expression of E-cadherin and N-cadherin was verified in the EMT models. β-Actin was used to normalize protein expression. b, d Western blot analysis of EMT markers (E-cadherin, N-cadherin, and vimentin) in the PCDHGA9 knockdown or overexpression cells compared with the control group. GAPDH was used to normalize protein expression. e Immunofluorescence showed that E-cadherin and N-cadherin expression levels were strengthened or weakened, respectively, in PCDHGA9-overexpressing SGC-7901 cells via laser confocal microscopy. f Western blot suggested that TGF-β induced EMT, upregulated N-cadherin, Snail and pSmad2/3, downregulated E-cadherin and did not alter Smad2/3 expression significantly, whereas overexpression of PCDHGA9 weakened this tendency and inhibited EMT in GC cells. GAPDH was used to normalize protein expression. g Immunofluorescence analysis via laser confocal microscopy indicated that overexpression of PCDHGA9 could decrease the phosphorylation of Smad2 and suppress the nuclear translocation of pSmad2 (*p < 0.05 and **p < 0.01)