Duan Qiaobin, Cai Lianxu, Zheng Kehong, Cui Chunhui, Huang Renli, Zheng Zheng, Xie Lang, Wu Cheng, Yu Xiang, Yu Jinlong
Department of Hernia and Abdominal Surgery, The First People's Hospital of FoShan, Affiliated FoShan Hospital of Sun Yat-sen University, Guangdong, Foshan 528000, P.R. China.
Department of General Surgery, Zhujiang Hospital, Southern Medical University, Guangdong, Guangzhou 510282, P.R. China.
Oncol Lett. 2020 Jul;20(1):601-610. doi: 10.3892/ol.2020.11619. Epub 2020 May 13.
Colorectal cancer (CRC) is one of the most common primary malignancies worldwide. Numerous studies have demonstrated that long non-coding RNAs (lncRNAs) are considered as crucial regulators of tumor progression. In particular, upregulation of the lncRNA KCNQ1OT1 was reported in various types of malignancy as a promoter of tumor progression. However, the role and underlying mechanism of KCNQ1OT1 in CRC remain unclear. Thus, the present study aimed to investigate the role of KCNQ1OT1 in colorectal cancer through GEPIA, reverse transcription-quantitative PCR (RT-qPCR) and western blot analyses, and cell assays. GEPIA analysis demonstrated that high expression levels of KCNQ1OT1 in CRC tissues predicted a poor prognosis for patients with CRC. KCNQ1OT1 was overexpressed in CRC tissues and cell lines via RT-qPCR analysis. Furthermore, the results from the cell viability assay, colony formation assay, wound healing assay, invasion assay and flow cytometric analysis demonstrated that KCNQ1OT1 knockdown significantly inhibited CRC cell proliferation, migration and invasiveness, and promoted CRC cell apoptosis, leading to cell cycle arrest. Western blot analysis demonstrated that KCNQ1OT1 knockdown inhibited the PI3K/AKT signaling pathway. These results suggest that KCNQ1OT1 may act as an oncogene through the PI3K/AKT signaling pathway in CRC.
结直肠癌（CRC）是全球最常见的原发性恶性肿瘤之一。大量研究表明，长链非编码RNA（lncRNAs）被认为是肿瘤进展的关键调节因子。特别是，lncRNA KCNQ1OT1在各种类型的恶性肿瘤中上调，被报道为肿瘤进展的促进因子。然而，KCNQ1OT1在结直肠癌中的作用及潜在机制仍不清楚。因此，本研究旨在通过基因表达谱交互分析（GEPIA）、逆转录定量PCR（RT-qPCR）、蛋白质免疫印迹分析及细胞实验，探究KCNQ1OT1在结直肠癌中的作用。GEPIA分析表明，结直肠癌组织中KCNQ1OT1的高表达预示着结直肠癌患者预后不良。通过RT-qPCR分析发现，KCNQ1OT1在结直肠癌组织和细胞系中过表达。此外，细胞活力测定、集落形成测定、伤口愈合测定、侵袭测定及流式细胞术分析结果表明，敲低KCNQ1OT1可显著抑制结直肠癌细胞的增殖、迁移和侵袭能力，并促进结直肠癌细胞凋亡，导致细胞周期停滞。蛋白质免疫印迹分析表明，敲低KCNQ1OT1可抑制PI3K/AKT信号通路。这些结果表明，KCNQ1OT1可能通过PI3K/AKT信号通路在结直肠癌中发挥癌基因作用。
