lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling
Authors Xiang C, Zhang Y, Zhang Y, Liu C, Hou Y, Zhang Y
Received 17 January 2020
Accepted for publication 31 March 2020
Published 25 May 2020 Volume 2020:12 Pages 3845—3850
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Antonella D'Anneo
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 China
Correspondence: Yan Zhang
Department of Oncology IV, First Hospital of Shijiazhuang, No. 36 Fanxi Road, Shijiazhuang City, Hebei Province 050000, People’s Republic of China
Tel +86 133 1597 8336
Introduction: 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
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