Bing Zhuan1,2, Yuting Lu3, Qian Chen1,2, Xia Zhao1,2, Ping Li1,2, Qun Yuan1,2, Zhao Yang4. 1. Department of Respiratory Medicine, Ningxia Hui Autonomous Region People's Hospital, Yinchuan, Ningxia, China. 2. Department of Respiratory Medicine, The First Affiliated Hospital of Northwest University for Nationalities, Yinchuan, Ningxia, China. 3. Second Department of Internal Medicine, Luohe Hospital of Traditional Chinese Medicine, Luohe, Henan, China. 4. Department of Respiratory Medicine, Suzhou Science & Technology Town Hospital, Suzhou, Jiangsu, China.
Abstract
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.
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.
Authors: Varun Kesherwani; Mamta Shukla; Don W Coulter; J Graham Sharp; Shantaram S Joshi; Nagendra K Chaturvedi Journal: BMC Med Genomics Date: 2020-06-26 Impact factor: 3.063
Authors: Agnieszka Taracha-Wisniewska; Grzegorz Kotarba; Sebastian Dworkin; Tomasz Wilanowski Journal: Int J Mol Sci Date: 2020-11-22 Impact factor: 5.923