Evidence map›Paper›PMID 28514532›Full record

ReviewBritish journal of pharmacology2017

The Dickkopf1-cytoskeleton-associated protein 4 axis creates a novel signalling pathway and may represent a molecular target for cancer therapy.

Akira Kikuchi, Katsumi Fumoto, Hirokazu Kimura

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
2.0field-weighted citation impact, top 13% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Akira KikuchiDepartment of Biochemistry and Molecular Biology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID http://orcid.org/0000-0003-3378-9522
Katsumi FumotoDepartment of Biochemistry and Molecular Biology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Hirokazu KimuraDepartment of Biochemistry and Molecular Biology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Osaka Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dickkopf 1 (DKK1) is a secreted protein and antagonizes oncogenic Wnt signalling by binding to the Wnt co-receptor, low-density lipoprotein receptor-related protein 6. DKK1 has also been suggested to regulate its own signalling, associated with tumour aggressiveness. However, the underlying mechanism by which DKK1 promotes cancer cell proliferation has remained to be clarified for a long time. The cytoskeleton-associated protein 4 (CKAP4), originally identified as an endoplasmic reticulum membrane protein, was recently found to act as a novel DKK1 receptor. DKK1 stimulates cancer cell proliferation when CKAP4 is expressed on the cell surface membrane. Although there are no tyrosine residues in the intracellular region of CKAP4, CKAP4 forms a complex with PI3K upon the binding of DKK1, leading to the activation of Akt. Both DKK1 and CKAP4 are frequently expressed in pancreatic and lung tumours, and their simultaneous expression is negatively correlated with prognosis. Knockdown of CKAP4 in cancer cells and treatment of mice with the anti-CKAP4 antibody inhibit Akt activity in cancer cells and suppress xenograft tumour formation, suggesting that CKAP4 may represent a therapeutic target for cancers expressing both DKK1 and CKAP4. This review will provide details of the novel DKK1-CKAP4 signalling axis that promotes cancer proliferation and discuss the possibility of targeting this pathway in future cancer drug development. LINKED ARTICLES: This article is part of a themed section on WNT Signalling: Mechanisms and Therapeutic Opportunities. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.24/issuetoc.

Indexed as

Signal TransductionAnimalsCell ProliferationHumansIntercellular Signaling Peptides and ProteinsMembrane ProteinsMolecular Targeted TherapyNeoplasmsNeoplasms, ExperimentalCKAP4 protein, humanDKK1 protein, humanDkk1 protein, mouseIntercellular Signaling Peptides and ProteinsMembrane Proteins

Identifiers

PMID28514532
PMCPMC5727324
OpenAlexW2800108104

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.