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Linc00210 drives Wnt/β-catenin signaling activation and liver tumor progression through CTNNBIP1-dependent manner

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收录情况： ◇ SCIE

作者：
Xiaomin Fu[1,2] * ; Xiaoyan Zhu[2] * ; Fujun Qin[3] ; Yong Zhang[1] ; Jizhen Lin[4] ; Yuechao Ding[5] ; Zihe Yang[6] ; Yiman Shang[1] ; Li Wang[1] ; Qinxian Zhang[2] ; Quanli Gao[1] ;
机构： [1]Department of Cancer Biology Immunotherapy, The Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, 127 Dongming Road, Zhengzhou, Henan 450003, China. [2]Department of Histology and Embryology, College of Basic Medicine, Zhengzhou University, 100 Kexue Road, Zhengzhou, Henan 450052, China. [3]Department of Pathology, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA. [4]Department of Otolaryngology, Medical School, University of Minnesota, Twin Cities Campus, Minneapolis, MN 55414, USA. [5]Department of Hepatopancreatobiliary Surgery, The Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, Zhengzhou, Henan 450003, China. [6]Department of Nuclear Medicine, The Affiliated Beijing Anzhen Hospital of Capital Medical University, Capital Medical University, Beijing 100029, China.
出处：
DOI： 10.1186/s12943-018-0783-3
ISSN：

关键词： Copy number alterations CTNNBIP1 Linc00210 Liver TICs Wnt/β-catenin

摘要：
Background: Liver tumor initiating cells (TICs) have self-renewal and differentiation properties, accounting for tumor initiation, metastasis and drug resistance. Long noncoding RNAs are involved in many physiological and pathological processes, including tumorigenesis. DNA copy number alterations (CNA) participate in tumor formation and progression, while the CNA of lncRNAs and their roles are largely unknown. Methods: LncRNA CNA was determined by microarray analyses, realtime PCR and DNA FISH. Liver TICs were enriched by surface marker CD133 and oncosphere formation. TIC self-renewal was analyzed by oncosphere formation, tumor initiation and propagation. CRISPRi and ASO were used for lncRNA loss of function. RNA pulldown, western blot and double FISH were used to identify the interaction between lncRNA and CTNNBIP1. Results: Using transcriptome microarray analysis, we identified a frequently amplified long noncoding RNA in liver cancer termed linc00210, which was highly expressed in liver cancer and liver TICs. Linc00210 copy number gain is associated with its high expression in liver cancer and liver TICs. Linc00210 promoted self-renewal and tumor initiating capacity of liver TICs through Wnt/β-catenin signaling. Linc00210 interacted with CTNNBIP1 and blocked its inhibitory role in Wnt/β-catenin activation. Linc00210 silencing cells showed enhanced interaction of β-catenin and CTNNBIP1, and impaired interaction of β-catenin and TCF/LEF components. We also confirmed linc00210 copy number gain using primary hepatocellular carcinoma (HCC) samples, and found the correlation between linc00210 CNA and Wnt/β-catenin activation. Of interest, linc00210, CTNNBIP1 and Wnt/β-catenin signaling targeting can efficiently inhibit tumor growth and progression, and liver TIC propagation. Conclusion: With copy-number gain in liver TICs, linc00210 is highly expressed along with liver tumorigenesis. Linc00210 drives the self-renewal and propagation of liver TICs through activating Wnt/β-catenin signaling. Linc00210 interacts with CTNNBIP1 and blocks the combination between CTNNBIP1 and β-catenin, driving the activation of Wnt/β-catenin signaling. Linc00210-CTNNBIP1-Wnt/β-catenin axis can be targeted for liver TIC elimination. © 2018 The Author(s).

基金：
This work was supported by Henan Provincial Scientific and Technological project (No.162300410095), Henan Medical Science and Technique Foundation (No.201701030).
语种：
外文
被引次数：
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2017]版：
大类 | 2 区 医学
小类 | 2 区 生化与分子生物学 2 区 肿瘤学
最新[2023]版：
大类 | 1 区 医学
小类 | 1 区 生化与分子生物学 1 区 肿瘤学
JCR分区：
出版当年[2016]版：
Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Q1 ONCOLOGY
最新[2023]版：
Q1 ONCOLOGY Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2016版] 出版当年五年平均 出版前一年[2015版] 出版后一年[2017版]

第一作者：
第一作者机构： [1]Department of Cancer Biology Immunotherapy, The Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, 127 Dongming Road, Zhengzhou, Henan 450003, China. [2]Department of Histology and Embryology, College of Basic Medicine, Zhengzhou University, 100 Kexue Road, Zhengzhou, Henan 450052, China.
共同第一作者：
通讯作者：
通讯机构： [1]Department of Cancer Biology Immunotherapy, The Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, 127 Dongming Road, Zhengzhou, Henan 450003, China. [2]Department of Histology and Embryology, College of Basic Medicine, Zhengzhou University, 100 Kexue Road, Zhengzhou, Henan 450052, China.
推荐引用方式(GB/T 7714)：
Xiaomin Fu,Xiaoyan Zhu,Fujun Qin,et al.Linc00210 drives Wnt/β-catenin signaling activation and liver tumor progression through CTNNBIP1-dependent manner[J].MOLECULAR CANCER.2018,17(1):-.doi:10.1186/s12943-018-0783-3.
APA：
Xiaomin Fu,Xiaoyan Zhu,Fujun Qin,Yong Zhang,Jizhen Lin...&Quanli Gao.(2018).Linc00210 drives Wnt/β-catenin signaling activation and liver tumor progression through CTNNBIP1-dependent manner.MOLECULAR CANCER,17,(1)
MLA：
Xiaomin Fu,et al."Linc00210 drives Wnt/β-catenin signaling activation and liver tumor progression through CTNNBIP1-dependent manner".MOLECULAR CANCER 17..1(2018):-

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