Evidence map›Paper›PMID 29136406›Full record

ArticleBritish journal of cancer2018

The interaction between androgen receptor and semenogelin I: a synthetic LxxLL peptide antagonist inhibits the growth of prostate cancer cells.

Peng Li, Jinbo Chen, Eiji Kashiwagi, Taichi Mizushima, Bin Han, Satoshi Inoue, Hiroki Ide, Koji Izumi, Hiroshi Miyamoto

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Steroid receptor/coactivator binding inhibitors: An update.Molecular and cellular endocrinology · 2019
    Review
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

9 authors at 3 institutions in 1 country.

Peng LiDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Jinbo ChenDepartment of Pathology & Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Eiji KashiwagiDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Taichi MizushimaDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Bin HanDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Satoshi InoueDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Hiroki IdeDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Koji IzumiDepartment of Pathology & Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Hiroshi MiyamotoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Johns Hopkins University · USJohns Hopkins Medicine · USUniversity of Rochester Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe previously demonstrated that a seminal plasma protein, semenogelin I (SgI), functioned as an androgen receptor (AR) coactivator. Meanwhile, several short sequence motifs in AR coregulators, such as LxxLL (L=leucine), have been shown to mediate specific interactions with AR.

methodsWe investigated the role of the LxxLL motif within SgI in the interactions with AR and cell growth in prostate cancer lines in vitro.

resultsA full-length SgI with mutations in the motif (i.e., LxxAA; A=alanine) failed to significantly increase cell proliferation/migration as well as androgen-mediated AR transcription. Co-immunoprecipitation showed no physical interactions between AR and the mutant SgI. In addition, transfection of an 18-amino acid peptide of SgI containing LxxLL, but not LxxAA, resulted in considerable reduction in cell growth and prostate-specific antigen expression in LNCaP and C4-2 lines.

conclusionsThe LxxLL motif of SgI could be a novel therapeutic target for both androgen-sensitive and castration-resistant prostate cancers.

Indexed as

AlanineCell Line, TumorCell MovementCell ProliferationChloridesDihydrotestosteroneHumansLeucineMaleMutationPeptidesProstatic NeoplasmsReceptors, AndrogenSeminal Vesicle Secretory ProteinsTranscription, GeneticZinc CompoundsAlanineChloridesDihydrotestosteroneLeucinePeptidesReceptors, AndrogenSeminal Vesicle Secretory Proteinsseminal vesicle-specific antigenzinc chlorideZinc Compounds

Identifiers

PMID29136406
PMCPMC5808024
OpenAlexW2771052166

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.