Fig. 4

Genetic ablation of Shp2 in lung epithelial cells or pharmacological inhibition of Shp2 alleviates the CS- and CSE-induced EMT phenotypes in lung tissues and NCI-H292 cells. a-b Shp2 knockout in lung epithelial cells or Shp2 inhibitor – PHPS1 (3 mg/kg, i.p injection) reduces the CS-induced changes of E-cadherin and vimentin mRNA and protein expression in lung tissues. n = 8 mice/per group. ^#p < 0.05, ^##p < 0.01, ^###p < 0.001 compared with control (WT mice), *p < 0.05 compared with control (WT mice) with CS exposure. c-e Shp2 inhibitor – PHPS1 alleviates the CSE exposure induced changes of E-cadherin and vimentin mRNA and protein expression in a concentration-dependent manner in NCI-H292 cells. n = 3 per group. ^#p < 0.05, ^##p < 0.01 compared with control (WT mice), ^*p < 0.05, ^**p < 0.01 compared with control (WT mice) with CS exposure. f–h) Shp2 knockdown or MMP-9 inhibitor – SB-3CT (1 μM) alleviates the 2.5% CSE exposure induced changes of E-cadherin and vimentin protein expression in NCI-H292 cells. n = 3 per group. ^#p < 0.05, ^##p < 0.01, compared with control; ^*p < 0.05 compared with 2.5% CSE exposure. At least three independent experiments in vitro were completed for each group assessment. Data are presented as the mean ± SEM. Statistical significance is determined by one-way ANOVA followed by the Student-Newman-Keuls test