Objective To investigate the effect of PD98059 on epithelial-mesenchymal transition ( EMT) of transforming growth factor β1 ( TGF-β1)-induced human bronchial epithelial cells BEAS-2B and the possible molecular mechanism. Methods Human bronchial epithelial cells (BEAS-2B) were used for the BEAS-2B EMT model established with TGF-β1, and the ERK1 / 2 inhibitor PD98059 was used to explore whether inhibition of ERK/ MAPK signal transduction affects the EMT process. Immunofluorescence was used to detect the expression and location of α-SMA protein in the BEAS-2B airway remodeling model. CCK-8 assays were used to assess the cell survival rate. An Edu proliferation assay was used to assess cell proliferation. Transwell assays were used to assess cell migration. Western blott was used to detect the expression of EMT marker proteins and activation of the ERK/ MAPK pathway. Results Compared with the control group, α-SMA expression in the model group was increased, and α-SMA was expressed in the cytoplasm of BEAS- 2B cells. Cotreatment with 40 μmol / L PD98059 and 5 ng / mL TGF-β1 inhibited BEAS-2B cell growth (P<0. 05). There was no significant difference in Edu-positive cells among the three groups (P>0.05). Compared with the normal group, the number of migrating cells (P<0.05), expression of EMT marker proteins (P<0.05), and expression of p-ERK protein were increased in the model group (P<0.05). PD98059 significantly reduced the number of migrating cells (P<0.05) and inhibited the expression of EMT marker proteins ( P< 0.05) and activation of the ERK pathway ( P< 0.05). Conclusions TGF-β1 promotes the EMT of human bronchial epithelial cells via the ERK/ MAPK pathway. PD98059 inhibits EMT of bronchial epithelial cells by suppressing activation of the ERK/ MAPK pathway.