Open AccessActivating transcription factor 3 promotes malignance of lung cancer cells in vitro
Author(s) -
Li Xuebing,
Zhou Xuexia,
Li Yongwen,
Zu Lingling,
Pan Hongli,
Liu Boning,
Shen Wang,
Fan Yaguang,
Zhou Qinghua
Publication year - 2017
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.12421
Subject(s) - lung cancer , gene knockdown , atf3 , cancer research , medicine , activating transcription factor , cell cycle , cell growth , cancer cell , downregulation and upregulation , cancer , metastasis , cell , biology , pathology , cell culture , transcription factor , gene expression , gene , promoter , biochemistry , genetics
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.