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
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI