Wang Han, Luan Hairong, Zhan Tao, Liu Xia, Song Jie, Dai Haibing
First Clinical Medical College, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China.
Basic Medical College, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China.
Exp Ther Med. 2020 Feb;19(2):1439-1447. doi: 10.3892/etm.2019.8350. Epub 2019 Dec 19.
Long non-coding RNAs (lncRNAs) have been indicated to serve critical roles in cancer development and progression. Long intergenic non-protein coding RNA 70 (LINC00707) was recently reported to be an oncogene involved in the tumorigenesis of several types of human cancer. However, the clinical role, biological functions and molecular mechanism of LINC00707 in colorectal cancer (CRC) remain unclear. The aim of the present study was to investigate the biological effects and mechanism of LINC00707 in CRC. Reverse transcription-quantitative PCR was used to detect the expression levels of LINC00707 in 65 CRC tissue samples and CRC cell lines (HCT116, HT29 and SW480). Cell Counting Kit-8 and colony formation assays were performed to investigate the effects of LINC00707 on CRC cell proliferation. A dual-luciferase reporter assay was conducted to investigate the mechanisms of LINC00707 in CRC. The upregulation of LINC00707 expression was significantly associated with tumor size, stage and poor survival in patients with CRC. LINC00707 also acted as an independent prognostic factor for CRC. Functional analyses revealed that the knockdown of LINC00707 could inhibit CRC cell proliferation. Furthermore, bioinformatics analysis demonstrated that microRNA (miR)-485-5p could directly bind to LINC00707, which was confirmed by a dual-luciferase reporter assay. In conclusion, the upregulation of LINC00707 is associated with a shorter survival time in patients with CRC. Knockdown of LINC00707 may inhibit the proliferation of CRC cells by binding with miR-485-5p.
长链非编码RNA（lncRNAs）已被表明在癌症的发生和发展中发挥关键作用。长链基因间非蛋白质编码RNA 70（LINC00707）最近被报道为一种癌基因，参与多种类型人类癌症的肿瘤发生。然而，LINC00707在结直肠癌（CRC）中的临床作用、生物学功能和分子机制仍不清楚。本研究的目的是探讨LINC00707在CRC中的生物学效应和机制。采用逆转录定量PCR检测65例CRC组织样本和CRC细胞系（HCT116、HT29和SW480）中LINC00707的表达水平。进行细胞计数试剂盒-8和集落形成试验，以研究LINC00707对CRC细胞增殖的影响。进行双荧光素酶报告基因试验，以研究LINC00707在CRC中的作用机制。LINC00707表达上调与CRC患者的肿瘤大小、分期及不良生存显著相关。LINC00707也是CRC的独立预后因素。功能分析显示，敲低LINC00707可抑制CRC细胞增殖。此外，生物信息学分析表明，微小RNA（miR）-485-5p可直接与LINC00707结合，双荧光素酶报告基因试验证实了这一点。总之，LINC00707的上调与CRC患者较短的生存时间相关。敲低LINC00707可能通过与miR-485-5p结合来抑制CRC细胞的增殖。
