Abstract | AIM: METHODS: 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.
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Authors | Bing Zhuan, Yuting Lu, Qian Chen, Xia Zhao, Ping Li, Qun Yuan, Zhao Yang |
Journal | Journal of cellular biochemistry
(J Cell Biochem)
Vol. 120
Issue 10
Pg. 17616-17624
(10 2019)
ISSN: 1097-4644 [Electronic] United States |
PMID | 31119790
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2019 Wiley Periodicals, Inc. |
Chemical References |
- KLF4 protein, human
- Klf4 protein, mouse
- Kruppel-Like Factor 4
- Kruppel-Like Transcription Factors
- MIRN103 microRNA, human
- MicroRNAs
- RNA, Long Noncoding
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Topics |
- A549 Cells
- Animals
- Apoptosis
(genetics)
- Cell Movement
(genetics)
- Cell Proliferation
(genetics)
- Disease Progression
- Female
- Gene Expression Regulation, Neoplastic
(genetics)
- Humans
- Kruppel-Like Factor 4
- Kruppel-Like Transcription Factors
(genetics)
- Lung Neoplasms
(genetics, pathology)
- Male
- Mice
- MicroRNAs
(genetics)
- Neoplasm Invasiveness
(genetics, pathology)
- RNA, Long Noncoding
(genetics)
- Signal Transduction
(genetics)
- Xenograft Model Antitumor Assays
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