Evidence map›Paper›PMID 30004146›Full record

ArticleCell proliferation2018

β-catenin regulates IRF3-mediated innate immune signalling in colorectal cancer.

Chengming Ding, Jun He, Jun Zhao, Junhua Li, Jie Chen, Wenyan Liao, Yi Zeng, Jing Zhong, Chaoying Wei, Liming Zhang and 11 more

Erratum issuedOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  8. Review
  9. Identification of the Prognostic Value and Clinical Significance of Interferon Regulatory Factors (IRFs) in Colon Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 4 institutions in 2 countries.

Chengming DingDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, China.ORCID http://orcid.org/0000-0002-6979-1221
Jun HeDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital, University of South China, Hengyang, China.
Jun ZhaoDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA.
Junhua LiDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA.
Jie ChenDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, China.
Wenyan LiaoDepartment of Obstetrics and Gynecology, The First Affiliated Hospital, University of South China, Hengyang, China.
Yi ZengDepartment of Pathology and Immunology, Youjiang Medical University for Nationalities, Baise, China.
Jing ZhongInstitute of Clinical Medicine, The First Affiliated Hospital, University of South China, Hengyang, China.
Chaoying WeiThe State Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, China.
Liming ZhangThe State Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, China.
Mei ZhouThe State Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, China.
Zeming JiaDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, China.
Yaoting ZhangDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, China.
Hui LiThe State Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, China.
Yuzheng ZhouThe State Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, China.
Xiaolong XiaoThe State Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, China.
Dong HanDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital, University of South China, Hengyang, China.
Chong LiDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital, University of South China, Hengyang, China.
Zhu ZhuDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital, University of South China, Hengyang, China.
Zanxian XiaThe State Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, China.
Jian PengDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, China.ORCID http://orcid.org/0000-0003-0991-3896
Central South University · CNFirst Affiliated Hospital of University of South China · CNUniversity of Southern California · USAffiliated Hospital of Youjiang Medical University for Nationalities · CN

Funding

China Scholarship Council 201406370025Hunan Provincial Natural Science Fund 2017JJ2334Hunan Provincial Natural Science Fund 2018JJ3471Joint Funds of the National Natural Science Foundation of China U1603126National Key Research and Development Program of China 2016YFC1200200National Key Research and Development Program of China 2016YFD0500300
6 · The paper itself

Abstract

objectiveβ-catenin is one of the most critical oncogenes associated with many kinds of human cancers, especially in the human CRC. Innate immunity recognizes tumour derived damage-associated molecular patterns (DAMPs) and primes the anti-tumour adaptive responses. While the function of β-catenin in CRC tumourigenesis is well established, its impact on innate immune evasion is largely unknown. The aim of this study is to characterize the role of β-catenin in inhibiting RIG-I-like receptor (RLR)-mediated IFN-β signalling in colorectal cancer. MATERIALS AND

methodsImmunohistochemical staining and western blotting were conducted to study the expression of β-catenin, IRF3 and phospho-IRF3 (p-IRF3) in CRC samples and cell lines. Plaque assay determining virus replication was performed to assess the regulation of β-catenin on IFN-β signalling. The inhibition of β-catenin on RLR-mediated IFN-β signalling was further studied by real-time analyses and reporter assays in the context of lentiviral-mediated β-catenin stably knocking down. Lastly, co-immunoprecipitation and nuclear fractionation assay were conducted to monitor the interaction between β-catenin and IRF3.

resultsWe found that high expression of β-catenin positively correlated with the expression of IRF3 in CRC cells. Overexpression of β-catenin increased the viral replication. Conversely knocking down of β-catenin inhibited viral replication. Furthermore, our data demonstrated that β-catenin could inhibit the expression of IFN-β and interferon-stimulated gene 56 (ISG56). Mechanistically, we found that β-catenin interacted with IRF3 and blocked its nuclear translocation.

conclusionOur study reveals an unprecedented role of β-catenin in enabling innate immune evasion in CRC.

Indexed as

AdultAgedAged, 80 and overAnimalsbeta CateninCell LineChlorocebus aethiopsColorectal NeoplasmsFemaleHCT116 CellsHEK293 CellsHT29 CellsHumansImmunity, InnateImmunoprecipitationInterferon-betabeta CateninInterferon-betaInterferon Regulatory Factor-3IRF3 protein, humanTranscription Factorscolorectal cancerinnate immunityIRF3RIG-I-like receptor (RLR)-mediated IFN-β signalling pathwayβ-catenin

Identifiers

PMID30004146
PMCPMC6528881
OpenAlexW2884300981

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.