Long non-coding RNAs (lncRNAs) have shown to act as important regulators in cancer biology. The aim of this study was to investigate the role and mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in colorectal cancer (CRC) progression. The abundance of KCNQ1OT1, microRNA-216b-5p (miR-216b-5p) and zinc finger protein 146 (ZNF146) messenger RNA (mRNA) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Cell migration and invasion abilities were assessed by transwell assays. Western blot assay was performed for determination of protein levels. LncBase v.2 of DIANA Tool and StarBase software were used to predict the targets of KCNQ1OT1 and miR-216b-5p, respectively. Dual-luciferase reporter assay was implemented to confirm the target interaction between miR-216b-5p and KCNQ1OT1 or ZNF146. KCNQ1OT1 expression was higher in CRC tissues and cell lines. KCNQ1OT1 interference restrained the proliferation, migration and invasion of CRC cells. MiR-216b-5p was a target of KCNQ1OT1 in CRC cells, and KCNQ1OT1 knockdown-induced effects in CRC cells were partly overturned by miR-216b-5p silencing. MiR-216b-5p bound to the 3′ untranslated region (3′UTR) of ZNF146, and ZNF146 overexpression partly attenuated miR-216b-5p overexpression-mediated influences in CRC cells. KCNQ1OT1 up-regulated the abundance of ZNF146 through sequestering miR-216b-5p in CRC cells. KCNQ1OT1 accelerated the proliferation and motility of CRC cells through elevating ZNF146 expression via sponging miR-216b-5p. KCNQ1OT1/miR-216b-5p/ZNF146 axis might be underlying target for the diagnosis and treatment of CRC patients.

长链非编码 RNA (lncRNA) 已显示在癌症生物学中充当重要的调节剂。本研究的目的是研究 lncRNA KCNQ1 相反链/反义转录物 1 (KCNQ1OT1) 在结直肠癌 (CRC) 进展中的作用和机制。通过定量实时聚合酶链反应 (qRT-PCR) 测量 KCNQ1OT1、microRNA-216b-5p (miR-216b-5p) 和锌指蛋白 146 (ZNF146) 信使 RNA (mRNA) 的丰度。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑 (MTT) 测定和集落形成测定分析细胞增殖。通过transwell测定评估细胞迁移和侵袭能力。进行蛋白质印迹测定以确定蛋白质水平。DIANA Tool 的 LncBase v.2 和 StarBase 软件分别用于预测 KCNQ1OT1 和 miR-216b-5p 的靶点。实施双荧光素酶报告基因检测以确认 miR-216b-5p 与 KCNQ1OT1 或 ZNF146 之间的靶标相互作用。KCNQ1OT1 在 CRC 组织和细胞系中的表达较高。KCNQ1OT1干扰抑制了CRC细胞的增殖、迁移和侵袭。MiR-216b-5p 是 CRC 细胞中 KCNQ1OT1 的靶标，并且 KCNQ1OT1 敲低在 CRC 细胞中诱导的作用被 miR-216b-5p 沉默部分推翻。MiR-216b-5p 与 ZNF146 的 3' 非翻译区 (3'UTR) 结合，ZNF146 过表达部分减弱了 CRC 细胞中 miR-216b-5p 过表达介导的影响。KCNQ1OT1 通过隔离 CRC 细胞中的 miR-216b-5p 上调 ZNF146 的丰度。KCNQ1OT1 通过海绵 miR-216b-5p 提高 ZNF146 表达来加速 CRC 细胞的增殖和运动。