Beclin 1 promotes apoptosis and decreases invasion by upregulating the expression of ECRG4 in A549 human lung adenocarcinoma cells.

Although Beclin 1 has been demonstrated to exert an important role in cell autophagy during carcinogenesis, its biological function in lung cancer has yet to be fully elucidated. A previous study by our laboratory identified that knockdown of Beclin 1 promoted cell growth and inhibited apoptosis in the A549 lung cancer cell line. In the present study, a Beclin 1 lentiviral expression vector was constructed, and an A549 cell line was established with a steady expression of Beclin 1. Furthermore, the effect of Beclin 1 overexpression on cell invasion and apoptosis, changes in the activities of the apoptosis-associated caspases-3 and -9, and the overexpression of esophageal cancer-related gene 4 (ECRG4) were examined. The results demonstrated that the overexpression of Beclin 1 in A549 cells reduced cell invasion by Matrigel invasion assay and promoted apoptosis by flow cytometric analysis (P<0.01) compared with Lenex-packaged lentiviral particles and non-transfected control groups. Furthermore, the overexpression of Beclin 1 in A549 cells increased the activities of caspases-3 and -9 and the expression of ECRG4 (P<0.01) compared with Lenex-packaged lentiviral particles and non-transfected control groups. In conclusion, the overexpression of Beclin 1 promoted apoptosis and decreased invasion by upregulating the expression of ECRG4 in A549 lung adenocarcinoma cells. Therefore, the selection of Beclin 1 as a target for gene therapy represents a more effective method for the treatment of lung cancer.