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.

中文翻译：

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LncRNA TUG1通过海绵miR-1294调节PLK1表达促进食管癌发展

目的食管癌是生存率低的恶性肿瘤之一。由于有限的治疗选择和耐药性的发展，食管癌患者的 5 年生存率仍然很低。最近的证据表明长链非编码RNA（lncRNA）参与了肿瘤的发生和发展，然而，lncRNA牛磺酸上调基因1（TUG1）在食管癌中的分子机制尚不清楚。结果 TUG1 在食管癌组织和细胞中过度表达。敲低 TUG1 抑制增殖和侵袭，同时通过负调节 miR-1294 表达促进食管癌细胞凋亡。此外，PLK1是食管癌细胞中miR-1294的靶mRNA。因此，PLK1 沉默对增殖、凋亡、通过沉默 miR-1294 可以逆转食管癌细胞的侵袭和侵袭。此外，TUG1 沉默抑制了体内肿瘤细胞的生长。结论 TUG1是食管癌的致癌基因。从机制上讲，TUG1 通过调节 miR-1294/PLK1 轴将其归因于食管癌过程。