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Overexpression of the long noncoding RNA TRHDE‐AS1 inhibits the progression of lung cancer via the miRNA‐103/KLF4 axis
Author(s) -
Zhuan Bing,
Lu Yuting,
Chen Qian,
Zhao Xia,
Li Ping,
Yuan Qun,
Yang Zhao
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29029
Subject(s) - klf4 , microrna , biology , cancer research , cell growth , long non coding rna , messenger rna , rna , microbiology and biotechnology , cell , lung cancer , gene , genetics , pathology , embryonic stem cell , sox2 , medicine
Aim The aim of this study was to explore the role and molecular basis of the long noncoding RNA (lncRNA) TRHDE‐AS1 in lung cancer. Methods 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. Results 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. Conclusion 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.