Abstract: Objective To explore the mechanism of environmental carcinogen benzopyrene promoting the pathogenesis of lung cancer. Methods Human bronchial epithelium (HBE) cells and non-small cell lung cancer cell line H1299 were treated with benzopyrene (Bap) by different exposure doses (0 μmol/L, 2.5 μmol/L, 5 μmol/L, 10 μmol/ L), different exposure time (0 h, 6 h, 12 h, 24 h) and the presence or absence of BaP receptor AhR inhibitor α-NF，and the expressions of c-jun protein under the different conditions were evaluated. Results With the increase of BaP dose, the relative expressions of c-jun protein in HBE and H1299 were all increased from 0.04 (dose 0 μmol/L) to 0.84 (dose 10 μmol/L) (P＜ 0.01) and 0.91 (dose 0 μmol/L) to 1.3(dose 10 μmol/L) (P＜ 0.01)；with the increase of exposure time, the relative expressions of c-jun protein of HBE and H1299 were up-regulated from 0.08 (exposure time 0 h) to 0.87 (exposure time 24 h) (P＜ 0.01) and from 0.33 (exposure time 0 h) 0.58(exposure time 24 h) (P＜ 0.05).The expression of c-jun protein was positively related to the dose and exposure time of BaP.After adding AhR inhibitor α-NF, the expression of c-jun protein in the nucleus decreased from 2.1 to 0.7 (P＜ 0.05) in HBE cells. Conclusion In HBE and H1299 cell lines, the environmental carcinogen benzopyrene induced the malignant transformation of the cells by up-regulating the expression of proto-oncogene c-jun in a dose-department and time-department manner.