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lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling
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 pat...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7260488/ https://www.ncbi.nlm.nih.gov/pubmed/32547220 http://dx.doi.org/10.2147/CMAR.S246422 |
Sumario: | 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. |
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