已发表论文

lncRNA LEF1-AS1 通过调节 miR-221/PTEN 信号传导促进非小细胞肺癌细胞的增殖并诱导其细胞凋亡

 

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

DOI https://doi.org/10.2147/CMAR.S246422

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Antonella D'Anneo

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




Figure 1 LEF1-AS1 was upregulated in both LUAD and...