Figures & data
Figure 7 Celecoxib up-regulated E-cadherin via inhibition of COX-2–PGE2–EP2–p-Akt/p-ERK in Bel7402 cells. Compared with DMSO-treated and empty plasmid-transfected Bel7402 cells, overexpression of COX-2 by using COX-2 ORF plasmid induced reduction of E-cadherin expression and increase of p-Akt and p-ERK expression determined by IF (A) and Western blot (D). Compared with DMSO-treated cells, the expression of E-cadherin quantified by IF (B and C) and Western blot (E and F) was upregulated by EP2 inhibitor AH6809, Akt inhibitor MK2206, and ERK inhibitor AZD6244, but down-regulated by PGE2, which could be reversed by AH6809. Meanwhile, the expression of p-Akt and p-ERK was significantly suppressed by treatment with celecoxib and AH6809 but was enhanced by treatment with PGE2, which could be inhibited by AH6809 (E). Scale bar =50 μm for IF.
![Figure 7 Celecoxib up-regulated E-cadherin via inhibition of COX-2–PGE2–EP2–p-Akt/p-ERK in Bel7402 cells. Compared with DMSO-treated and empty plasmid-transfected Bel7402 cells, overexpression of COX-2 by using COX-2 ORF plasmid induced reduction of E-cadherin expression and increase of p-Akt and p-ERK expression determined by IF (A) and Western blot (D). Compared with DMSO-treated cells, the expression of E-cadherin quantified by IF (B and C) and Western blot (E and F) was upregulated by EP2 inhibitor AH6809, Akt inhibitor MK2206, and ERK inhibitor AZD6244, but down-regulated by PGE2, which could be reversed by AH6809. Meanwhile, the expression of p-Akt and p-ERK was significantly suppressed by treatment with celecoxib and AH6809 but was enhanced by treatment with PGE2, which could be inhibited by AH6809 (E). Scale bar =50 μm for IF.](/cms/asset/431455e5-129f-4853-aee0-cb0695569fb3/dcmr_a_12190092_f0001_c.jpg)