期刊
THORACIC CANCER
卷 8, 期 3, 页码 181-191出版社
WILEY
DOI: 10.1111/1759-7714.12421
关键词
ATF3; lung cancer; tumor progression
资金
- National Natural Science Foundation of China [81572288, 81302002, 81502166]
- Key Project of International Cooperation of Science and Technology Innovation between Governments
- National Key Research and Development Plan of China [2016YEE0103400]
- Tianjin Natural Science Foundation [14JCQNJC12300]
- Foundation of Tianjin Medical University [2014KYQ02]
- Foundation of Tianjin Medical University General Hospital [ZYYFY2014038, ZYYFY2016013]
- New Century Talent Training Project of Tianjin Medical University General Hospital
BackgroundLung 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 (ATF3) in various cancers suggests an oncogenic role; however, its function in lung cancer is largely unknown. MethodsSixty-four pairs of lung cancer tissues were collected for ATF3 expression analysis by quantitative real-time PCR, immunoblotting, and immunohistochemistry staining. Correlations between ATF3 expression with clinicopathological features and overall survival were analyzed. ATF3 expression in a panel of lung cancer cell lines together with normal bronchial epithelial Beas-2B cells was also determined. Human H1299 and A549 cells were used for ATF3 knockdown and/or overexpression assays. Alterations in cell proliferation, cell cycle attribution, migration, and invasion were all assessed in vitro. ResultsIncreased ATF3 messenger RNA and protein expression were observed in lung cancer tissues/cells compared with normal tissues/cells. High tumorous ATF3 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 ATF3 significantly inhibited the cell proliferation, cell cycle progression, migration, and invasion capacities of lung cancer cells in vitro, whereas forced expression of ATF3 did the opposite. ConclusionUpregulation of ATF3 in lung cancer promotes cell proliferation, migration, and invasion, and may represent a novel therapeutic target for lung cancer.
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