Fig. 3: PI3K/AKT pathway mediates signal transduction between GPR35 and KLF5.

A Pathway enrichment analysis of differentially expressed genes in KA treated GPR35 normal and deficient IECs based on KEGG database. B Western blot analysis of the activation of PI3K/AKT and MEK/ERK pathways in GPR35 normal and deficient IECs that were treated with KA for 48 h. C, D Effect of specific inhibition of PI3K phosphorylation using PF-04691502 (PF, 0.5 μmol/L) on KA-induced KLF5 protein (C) and mRNA (D) expression (n = 3). E, F Effect of specific inhibition of AKT and mTOR phosphorylation using MK-2206 (MK, 5 μmol/L) and Rapamycin (Rap, 0.5 μmol/L) respectively on KA-induced KLF5 protein (E) and mRNA (F) expression (n = 3). G−I Effect of specific inhibition of PI3K, AKT and mTOR phosphorylation respectively on KA-induced IECs proliferation (H), migration (I) and their related gene expression (G) (n = 3). Data are presented as means ± SD. Statistical analysis was performed using Student’s t test. *P < 0.05, **P < 0.01 and ***P < 0.001.