Long non-coding RNA MINCR aggravates colon cancer via regulating miR-708-5p-mediated Wnt/β-catenin pathway

Wnt信号通路 基因敲除 癌症研究 癌变 长非编码RNA 连环素 生物 结直肠癌 免疫印迹 细胞生长 核糖核酸 分子生物学 癌症 细胞培养 基因 细胞生物学 信号转导 遗传学
作者
Yang Yu,Zhuo Chang,Chao Han,Lingling Zhuang,Chongzhi Zhou,Xiaosheng Qi,Zhihai Peng
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier BV]
卷期号:129: 110292-110292 被引量:46
标识
DOI:10.1016/j.biopha.2020.110292
摘要

BACKGROUND: Increasing evidence has found that the dysregulation of long non-coding RNAs (lncRNAs) may be important indicators in tumorigenesis. MYC-induced long non-coding RNA (MINCR) has been found to be related with some cancers, such as non-small cell lung cancer and gallbladder cancer. Besides, MINCR has potentially prognostic value for colon cancer (CC) patients' prognosis, yet its function and molecular mechanism in CC are not explored. METHODS: qRT-PCR evaluated gene expression, and western blot detected protein level. In vitro and in vivo experiments were adopted to understand the biological role of MINCR in CC. TOP/FOP Flash assay was performed to measure the activity of Wnt/β-catenin pathway. RNA pull down, luciferase reporter and RIP assays were utilized to analyze the relationship among genes. Immunohistochemistry and HE staining techniques were utilized to evaluate Ki67 staining in xenografts. RESULTS: MINCR was up-regulated in CC cells. Knockdown of MINCR suppressed cell proliferation and migration. MINCR could up-regulate CTNNB1 via sequestering miR-708-5p, resulting in activated Wnt/β-catenin pathway. The addition of LiCl treatment, miR-708-5p inhibitor or pcDNA3.1/CTNNB1 abolished the inhibitory impacts induced by MINCR silence in CC progression. CONCLUSION: MINCR sponges miR-708-5p to up-regulate CTNNB1 and activate Wnt/β-catenin pathway, thus promoting the development CC. Targeting MINCR might shed new light on the therapeutic strategies of CC.

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