Conclusion
LEF1-AS1 may promote the proliferation and induce apoptosis of NSCLC cells by regulating miR-221/PTEN signaling.
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.