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Chen Xiang,1 Yuanli Zhang,2 Yajing Zhang,1 Ci Liu,1 Yuehong Hou,1 Yan Zhang1 1Department of Oncology IV, First Hospital of Shijiazhuang, Shijiazhuang City, Hebei Province 050000, People’s Republic of China; 2Department of Cardiology Ⅱ, First Hospital of Shijiazhuang, Shijiazhuang City, Hebei Province 050000, People’s Republic of ChinaCorrespondence: Yan ZhangDepartment of Oncology IV, First Hospital of Shijiazhuang, No. 36 Fanxi Road, Shijiazhuang City, Hebei Province 050000, People’s Republic of ChinaTel +86 133 1597 8336Email zv5087@163.comIntroduction: LEF1-AS1 is a characterized oncogenic lncRNA in oral cancer. Analysis of TCGA dataset revealed the upregulation of LEF1-AS1 in non-small-cell lung cancer (NSCLC). This study was therefore carried out to investigate the involvement of LEF1-AS1 in NSCLC.Methods: A total of 62 NSCLC patients were included to collect paired cancer and non-tumor tissues. RT-qPCR was performed to measure levels of LEF1-AS1 and miR-221 expression. Transient transfections were performed to explore the interactions between LEF1-AS1, miR-221 and PTEN. Cell proliferation and apoptosis were analyzed by cell proliferation assay and cell apoptosis assay, respectively.Results: We found that LEF1-AS1 was upregulated in NSCLC patients. In addition, expression of LEF1-AS1 was negatively correlated with the expression of PTEN but positively correlated with the expression of miR-221 in NSCLC tissue samples. In NSCLC cells, overexpression of LEF1-AS1 led to downregulated expression of PTEN but upregulated expression of miR-221, which can directly target PTEN. Overexpression of LEF1-AS1 and miR-221 promoted cancer cell proliferation and inhibited apoptosis. PTEN played an opposite role and reduced the effects of overexpressing LEF1-AS1 and miR-221.Conclusion: LEF1-AS1 may promote the proliferation and induce apoptosis of NSCLC cells by regulating miR-221/PTEN signaling.Keywords: non-small-cell lung cancer, LEF1-AS1, miR-221, PTEN