| Title |
RETRACTED ARTICLE: Linc00210 drives Wnt/β-catenin signaling activation and liver tumor progression through CTNNBIP1-dependent manner
|
|---|---|
| Published in |
Molecular Cancer, March 2018
|
| DOI | 10.1186/s12943-018-0783-3 |
| Pubmed ID | |
| Authors |
Xiaomin Fu, Xiaoyan Zhu, Fujun Qin, Yong Zhang, Jizhen Lin, Yuechao Ding, Zihe Yang, Yiman Shang, Li Wang, Qinxian Zhang, Quanli Gao |
| Abstract |
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. 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. 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. 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. |
X Demographics
The data shown below were collected from the profiles of 6 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 6 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 5 | 83% |
| Science communicators (journalists, bloggers, editors) | 1 | 17% |
Mendeley readers
The data shown below were compiled from readership statistics for 25 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 25 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 6 | 24% |
| Student > Doctoral Student | 3 | 12% |
| Student > Master | 3 | 12% |
| Professor > Associate Professor | 2 | 8% |
| Student > Bachelor | 1 | 4% |
| Other | 0 | 0% |
| Unknown | 10 | 40% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 5 | 20% |
| Agricultural and Biological Sciences | 3 | 12% |
| Pharmacology, Toxicology and Pharmaceutical Science | 2 | 8% |
| Biochemistry, Genetics and Molecular Biology | 1 | 4% |
| Economics, Econometrics and Finance | 1 | 4% |
| Other | 3 | 12% |
| Unknown | 10 | 40% |
Attention Score in Context
This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 17 January 2019.
All research outputs
#13,582,950
of 23,028,364 outputs
Outputs from Molecular Cancer
#836
of 1,733 outputs
Outputs of similar age
#173,235
of 333,763 outputs
Outputs of similar age from Molecular Cancer
#24
of 53 outputs
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