Zhai Hui-Yuan, Sui Ming-Hua, Yu Xiao, Qu Zhen, Hu Jin-Chen, Sun Hai-Qing, Zheng Hai-Tao, Zhou Kai, Jiang Li-Xin
Department of Gastrointestinal Surgery, Yantai Yuhuangding Hospital, Yantai, Shandong, China (mainland).
Department of Oncology, Yantai Yuhuangding Hospital, Yantai, Shandong, China (mainland).
Med Sci Monit. 2016 Sep 16;22:3281-7. doi: 10.12659/msm.897072.
BACKGROUND Colon cancer is one of the most prevalent and deadly cancers worldwide. It is still necessary to further define the mechanisms and explore therapeutic targets of colon cancer. Dysregulation of long noncoding RNAs (lncRNAs) has been shown to be correlated with diverse biological processes, including tumorigenesis. This study aimed to characterize the biological mechanism of taurine-upregulated gene 1 (TUG1) in colon cancer. MATERIAL AND METHODS qRT-PCR was used to analyze the expression level of TUG1 and p63 in 75 colon cancer tissues and the matched adjacent non-tumor tissue. In vitro, cultured colon cancer cell lines HCT-116 and LoVo were used as cell models. TUG1 and p63 were silenced via transferring siRNA into HCT-116 or LoVo. The effects of TUG1 were investigated by examining cell proliferation, apoptosis, and migration. RESULTS Among the 75 colon cancer cases, the expression of TUG1 was significantly higher in colon cancer tissues compared with the matched adjacent non-tumor tissue, while p63 expression was lower in the tumor tissue. In HCT-116 and LoVo, the expression of TUG1 was significantly increased by p63 siRNA transfection. Furthermore, down-regulation of TUG1 by siRNA significantly inhibited the cell proliferation and promoted colon cancer cell apoptosis. In addition, inhibition of TUG1 expression significantly blocked the cell migration ability of colon cancer cells. CONCLUSIONS LncRNA TUG1 may serve as a potential oncogene for colon cancer. Overexpressed TUG1 may contribute to promoting cell proliferation and migration in colon cancer cells.
结肠癌是全球最常见且致命的癌症之一。进一步明确结肠癌的发病机制并探索其治疗靶点仍很有必要。长链非编码RNA（lncRNA）的失调已被证明与多种生物学过程相关，包括肿瘤发生。本研究旨在阐明牛磺酸上调基因1（TUG1）在结肠癌中的生物学机制。
采用qRT-PCR分析75例结肠癌组织及配对的癌旁非肿瘤组织中TUG1和p63的表达水平。体外实验中，以培养的结肠癌细胞系HCT-116和LoVo作为细胞模型。通过向HCT-116或LoVo细胞转染小干扰RNA（siRNA）来沉默TUG1和p63。通过检测细胞增殖、凋亡和迁移来研究TUG1的作用。
在75例结肠癌病例中，与配对的癌旁非肿瘤组织相比，结肠癌组织中TUG1的表达显著升高，而肿瘤组织中p63的表达较低。在HCT-116和LoVo细胞中，p63 siRNA转染显著增加了TUG1的表达。此外，siRNA下调TUG1显著抑制细胞增殖并促进结肠癌细胞凋亡。此外，抑制TUG1表达显著阻断结肠癌细胞的迁移能力。
lncRNA TUG1可能是结肠癌的潜在癌基因。TUG1过表达可能有助于促进结肠癌细胞的增殖和迁移。
