Activating transcription factor 3 promotes malignance of lung cancer cells in vitro

Background Lung cancer remains the most common cause of cancer‐related death, with high rates of recurrence and poor outcomes. An abnormally high expression of activating transcription factor 3 ( ATF 3) in various cancers suggests an oncogenic role; however, its function in lung cancer is largely unknown. Methods Sixty‐four pairs of lung cancer tissues were collected for ATF 3 expression analysis by quantitative real‐time PCR, immunoblotting, and immunohistochemistry staining. Correlations between ATF 3 expression with clinicopathological features and overall survival were analyzed. ATF 3 expression in a panel of lung cancer cell lines together with normal bronchial epithelial B eas‐2 B cells was also determined. Human H 1299 and A 549 cells were used for ATF 3 knockdown and/or overexpression assays. Alterations in cell proliferation, cell cycle attribution, migration, and invasion were all assessed in vitro . Results Increased ATF 3 messenger RNA and protein expression were observed in lung cancer tissues/cells compared with normal tissues/cells. High tumorous ATF 3 expression was significantly correlated with positive advanced tumor grade, lymph node metastasis, and shorter overall survival. Experimentally, we found that RNA interference mediated knockdown of ATF 3 significantly inhibited the cell proliferation, cell cycle progression, migration, and invasion capacities of lung cancer cells in vitro , whereas forced expression of ATF 3 did the opposite. Conclusion Upregulation of ATF 3 in lung cancer promotes cell proliferation, migration, and invasion, and may represent a novel therapeutic target for lung cancer.