Evidence map›Paper›PMID 28599655›Full record

ArticleBMC veterinary research2017

Canine REIC/Dkk-3 interacts with SGTA and restores androgen receptor signalling in androgen-independent prostate cancer cell lines.

Yuiko Kato, Kazuhiko Ochiai, Shota Kawakami, Nobuhiro Nakao, Daigo Azakami, Makoto Bonkobara, Masaki Michishita, Masami Morimatsu, Masami Watanabe, Toshinori Omi

Open access · goldAbstract read
In one paragraph

Article in BMC veterinary research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. The roles of cytosolic quality control proteins, SGTA and the BAG6 complex, in disease.Advances in protein chemistry and structural biology · 2019
    Review
  4. 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

10 authors at 3 institutions in 1 country.

Yuiko KatoSchool of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, 180-8602, Japan.
Kazuhiko OchiaiSchool of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, 180-8602, Japan. kochiai@nvlu.ac.jp.ORCID http://orcid.org/0000-0002-5736-0598
Shota KawakamiSchool of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, 180-8602, Japan.
Nobuhiro NakaoLaboratory of Animal Physiology, School of Animal Science, Nippon Veterinary and Life Science University, Tokyo, 180-8602, Japan.
Daigo AzakamiSchool of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, 180-8602, Japan.
Makoto BonkobaraDepartment of Veterinary Clinical Pathology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, 180-8602, Japan.
Masaki MichishitaDepartment of Veterinary Pathology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, 180-8602, Japan.
Masami MorimatsuLaboratory of Laboratory Animal Science and Medicine, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, 060-0818, Japan.
Masami WatanabeDepartment of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8558, Japan.
Toshinori OmiSchool of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, 180-8602, Japan. t.omi@nvlu.ac.jp.
Nippon Veterinary and Life Science University · JPHokkaido University · JPOkayama University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe pathological condition of canine prostate cancer resembles that of human androgen-independent prostate cancer. Both canine and human androgen receptor (AR) signalling are inhibited by overexpression of the dimerized co-chaperone small glutamine-rich tetratricopeptide repeat-containing protein α (SGTA), which is considered to cause the development of androgen-independency. Reduced expression in immortalised cells (REIC/Dkk-3) interferes with SGTA dimerization and rescues AR signalling. This study aimed to assess the effects of REIC/Dkk-3 and SGTA interactions on AR signalling in the canine androgen-independent prostate cancer cell line CHP-1.

resultsMammalian two-hybrid and Halo-tagged pull-down assays showed that canine REIC/Dkk-3 interacted with SGTA and interfered with SGTA dimerization. Additionally, reporter assays revealed that canine REIC/Dkk-3 restored AR signalling in both human and canine androgen-independent prostate cancer cells. Therefore, we confirmed the interaction between canine SGTA and REIC/Dkk-3, as well as their role in AR signalling.

conclusionsOur results suggest that this interaction might contribute to the development of a novel strategy for androgen-independent prostate cancer treatment. Moreover, we established the canine androgen-independent prostate cancer model as a suitable animal model for the study of this type of treatment-refractory human cancer.

Indexed as

Signal TransductionAnimalsCarrier ProteinsCell Line, TumorDisease Models, AnimalDog DiseasesDogsHumansIntercellular Signaling Peptides and ProteinsMaleProstatic NeoplasmsReceptors, AndrogenTumor Suppressor ProteinsCarrier ProteinsIntercellular Signaling Peptides and ProteinsReceptors, AndrogenTumor Suppressor ProteinsAndrogen receptor (AR) signallingCanineProstate cancerReduced expression in immortalised cells (REIC/Dkk-3)Small glutamine-rich tetratricopeptide repeat-containing protein α (SGTA)

Identifiers

PMID28599655
PMCPMC5466802
OpenAlexW2623701110

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.