Evidence map›Paper›PMID 25596747›Full record

ArticleOncotarget2015

Cathelicidin, an antimicrobial peptide produced by macrophages, promotes colon cancer by activating the Wnt/β-catenin pathway.

Dong Li, Wenfang Liu, Xuan Wang, Junlu Wu, Wenqiang Quan, Yiwen Yao, Robert Bals, Shurong Ji, Kaiyin Wu, Jia Guo and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 19% 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, 20 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. UropathogenicProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Dong LiDepartment of Clinical Laboratory, Tongji Hospital of Tongji University, 200065 Shanghai, China.
Wenfang LiuDepartment of General Surgery, Tongji Hospital of Tongji University, 200065 Shanghai, China.
Xuan WangDepartment of Pharmacy, Putuo People's Hospital, 200060 Shanghai, China.
Junlu WuDepartment of Clinical Laboratory, Tongji Hospital of Tongji University, 200065 Shanghai, China.
Wenqiang QuanDepartment of Clinical Laboratory, Tongji Hospital of Tongji University, 200065 Shanghai, China.
Yiwen YaoDepartment of Clinical Laboratory, Tongji Hospital of Tongji University, 200065 Shanghai, China.
Robert BalsDepartment of Internal Medicine V - Pulmonology, Allergology, Respiratory Intensive Care Medicine, Saarland University Hospital, 66424 Homburg, Germany.
Shurong JiDepartment of General Surgery, Tongji Hospital of Tongji University, 200065 Shanghai, China.
Kaiyin WuInstitute of Pathology, Charité University Hospital, 12200 Berlin, Germany.
Jia GuoTongji University Suzhou Institute, 215000 Suzhou, China.
Haiying WanDepartment of Clinical Laboratory, Tongji Hospital of Tongji University, 200065 Shanghai, China.
Tongji University · CNTongji Hospital · CNCentral Hospital of Putuo District · CNCharité - Universitätsmedizin Berlin · DESaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here we found that levels of cathelicidin, an antimicrobial peptide, were increased in colon cancer tissues compared to noncancerous tissues. Importantly, cathelicidin was mainly expressed in immune cells. Contact with tumor cells caused macrophages to secrete cathelicidin. Neutralization of cathelicidin, in vivo, significantly reduced the engraftment of macrophages into colon tumors, as well as proliferation of tumor cells, resulting in an inhibition of tumor growth. Furthermore, treatment with cathelicidin neutralizing antibody de-activated the Wnt/β-catenin signaling pathway in tumor cells both in vivo and in vitro. Cathelicidin activated Wnt/β-catenin signaling by inducing phosphorylation of PTEN, leading to activation of PI3K/Akt signaling and subsequent phosphorylation of GSK3β, resulting in stabilization and nuclear translocation of β-catenin. These data indicate that cathelicidin, expressed by immune cells in the tumor microenvironment, promotes colon cancer growth through activation of the PTEN/PI3K/Akt and Wnt/β-catenin signaling pathways.

Indexed as

Paracrine CommunicationWnt Signaling PathwayAnimalsAntibodies, NeutralizingAntimicrobial Cationic Peptidesbeta CateninCase-Control StudiesCathelicidinsCell ProliferationCell Transformation, NeoplasticCoculture TechniquesColitisColonic NeoplasmsDisease Models, AnimalFemaleGlycogen Synthase Kinase 3Antibodies, NeutralizingAntimicrobial Cationic Peptidesbeta CateninCathelicidinsCTNNB1 protein, humanCTNNB1 protein, mouseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mousePhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID25596747
PMCPMC4413629
OpenAlexW1565911218

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.