Mingzhu Zong1, Wanting Feng1, Li Wan1, Xiaojuan Yu1, Weiyong Yu2. 1. Department of Oncology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No. 6, West Beijing Road, Huai'an, 223300, Jiangsu, China. 2. Department of Oncology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No. 6, West Beijing Road, Huai'an, 223300, Jiangsu, China. nyucuanxuesilnq@163.com.
Abstract
OBJECTIVES: Esophageal cancer is one of the malignant tumor with poor survival. The 5-year survival rate of esophageal cancer patients remains poor due to limited therapeutic options and the development of drug-resistance. Recent evidence suggests that long non-coding RNAs (lncRNAs) are involved in occurrence and development of tumor, however, the molecular mechanisms of lncRNA taurine-upregulated gene 1 (TUG1) in esophageal cancer remain unknown. RESULTS: TUG1 was overexpressed in esophageal cancer tissues and cells. The knockdown of TUG1 repressed proliferation and invasion, while promoted apoptosis of esophageal cancer cells by negatively regulating miR-1294 expression. Furthermore, PLK1 was a target mRNA of miR-1294 in esophageal cancer cells. Therefore, the effects of PLK1 silencing on proliferation, apoptosis, and invasion of esophageal cancer cells could be overturned by silencing miR-1294. Additionally, TUG1 silencing inhibited growth of tumor cells in vivo. CONCLUSIONS: TUG1 was found as oncogenic gene in esophageal cancer. Mechanically, TUG1 attributed to esophageal cancer process by regulating miR-1294/ PLK1 axis.
OBJECTIVES: Esophageal cancer is one of the malignant tumor with poor survival. The 5-year survival rate of esophageal cancerpatients remains poor due to limited therapeutic options and the development of drug-resistance. Recent evidence suggests that long non-coding RNAs (lncRNAs) are involved in occurrence and development of tumor, however, the molecular mechanisms of lncRNA taurine-upregulated gene 1 (TUG1) in esophageal cancer remain unknown. RESULTS:TUG1 was overexpressed in esophageal cancer tissues and cells. The knockdown of TUG1 repressed proliferation and invasion, while promoted apoptosis of esophageal cancer cells by negatively regulating miR-1294 expression. Furthermore, PLK1 was a target mRNA of miR-1294 in esophageal cancer cells. Therefore, the effects of PLK1 silencing on proliferation, apoptosis, and invasion of esophageal cancer cells could be overturned by silencing miR-1294. Additionally, TUG1 silencing inhibited growth of tumor cells in vivo. CONCLUSIONS:TUG1 was found as oncogenic gene in esophageal cancer. Mechanically, TUG1 attributed to esophageal cancer process by regulating miR-1294/ PLK1 axis.