Abstract
The aim of this study was to explore the role and molecular basis of the long noncoding RNA (lncRNA) TRHDE-AS1 in lung cancer. We used real-time polymerase chain reaction to analyze the messenger RNA expression levels of TRHDE-AS1, miR-103, and KLF4. The cell viability, proliferation, and invasion rates were assessed via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, Cell Counting Kit-8, and Transwell assays to elucidate the role of TRHDE-AS1. Our results demonstrated that the lncRNA TRHDE-AS1 is mainly located in the cytoplasm and that the cell proliferation and invasion were suppressed in the group of overexpressed TRHDE-AS1. We also showed that miR-103 could directly bind to TRHDE-AS1 and provided evidence of the oncogenic function of miR-103. Besides, we proved that miR-103 exerted its function by adjusting the expression level of the tumor-suppressor gene KLF4, and the expression level was negatively associated with miR-103. In summary, we determined that the effects of TRHDE-AS1 on proliferation, invasion, and cell death could be rescued by the overexpression of miR-103. Our experiments demonstrate that the TRHDE-AS1/miR-103/KLF4 axis may provide new evidence for understanding the molecular basis of lung cancer.
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