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长链非编码RNA TUG1通过海绵吸附miR-1294调控PLK1表达促进食管癌发展。

LncRNA TUG1 promotes esophageal cancer development through regulating PLK1 expression by sponging miR-1294.

作者信息

Zong Mingzhu, Feng Wanting, Wan Li, Yu Xiaojuan, Yu Weiyong

机构信息

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.

出版信息

Biotechnol Lett. 2020 Dec;42(12):2537-2549. doi: 10.1007/s10529-020-02984-0. Epub 2020 Oct 2.

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.

摘要

目的

食管癌是一种生存率较低的恶性肿瘤。由于治疗选择有限和耐药性的发展,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仍不清楚。

结果

TUG1在食管癌组织和细胞中过表达。敲低TUG1可抑制食管癌细胞的增殖和侵袭,同时通过负调控miR-1294的表达促进其凋亡。此外,PLK1是食管癌细胞中miR-1294的靶mRNA。因此,沉默miR-1294可逆转PLK1沉默对食管癌细胞增殖、凋亡和侵袭的影响。此外,TUG1沉默在体内抑制肿瘤细胞生长。

结论

TUG1被发现是食管癌中的致癌基因。机制上,TUG1通过调节miR-1294/PLK1轴参与食管癌的发生发展过程。

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