Evidence map›Paper›PMID 33539321›Full record

ArticleAging2021

GV1001 interacts with androgen receptor to inhibit prostate cell proliferation in benign prostatic hyperplasia by regulating expression of molecules related to epithelial-mesenchymal transition.

Yejin Kim, Dahae Lee, Hyejung Jo, Cheolhyeon Go, Jongwon Yang, Dongmin Kang, Jae Seung Kang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  14. Neferine attenuates development of testosterone-induced benign prostatic hyperplasia in mice by regulating androgen and TGF-β/Smad signaling pathways.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  15. Effects of red ginseng oil(KGC11Journal of ginseng research · 2022
    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

7 authors at 3 institutions in 2 countries.

Yejin KimDepartment of Anatomy, Seoul National University College of Medicine, Seoul, Republic of Korea.
Dahae LeeDepartment of Anatomy, Seoul National University College of Medicine, Seoul, Republic of Korea.
Hyejung JoDepartment of Anatomy, Seoul National University College of Medicine, Seoul, Republic of Korea.
Cheolhyeon GoDepartment of Anatomy, Seoul National University College of Medicine, Seoul, Republic of Korea.
Jongwon YangDepartment of Anatomy, Seoul National University College of Medicine, Seoul, Republic of Korea.
Dongmin KangDepartment of Psychological and Brain Sciences, College of Arts and Sciences, Boston University, Boston, MA 02215, USA.
Jae Seung KangDepartment of Anatomy, Seoul National University College of Medicine, Seoul, Republic of Korea.
Seoul National University · KRBoston University · USSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cell proliferation, driven by testosterone, is a major characteristic of benign prostatic hyperplasia (BPH). GV1001, a human telomerase reverse transcriptase catalytic subunit, is an injectable formulation used as a cancer vaccine. It functions as a cell penetrating peptide to regulate cell proliferation. Here, we found that GV1001 effectively suppressed proliferation of prostatic stromal myofibroblasts (WPMY-1) and prostatic epithelial cells (RWPE-1 and WPE-NA22) treated with dihydrotestosterone. Also, GV1001 bound to androgen receptors (ARs) in the cytosol of stromal and epithelial cells. In an experimental animal model implanted with an infusion pump for spontaneous and continuous release of testosterone, revealed that GV1001 reduced prostatic hypertrophy and inhibited the cell proliferation and the expression of Ki67, proliferating cell nuclear antigen, and prostate specific antigen. In addition, GV1001 prevented fibrosis of the prostate by downregulating expression of prostatic epithelial-mesenchymal transition (EMT)-related proteins such as transforming growth factor (TGF)-β, Snail, Slug, N-cadherin, and Vimentin, and by up-regulating E-cadherin. Taken together, these results suggest that GV1001, which suppresses TGF-β-mediated EMT by outcompeting testosterone for binding to AR, is a potential therapeutic drug for BPH accompanied by prostatic fibrosis.

Indexed as

Receptors, AndrogenAnimalsCell LineCell ProliferationDihydrotestosteroneEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticMaleMiceMice, Inbred C57BLPeptide FragmentsProstatic HyperplasiaTelomeraseDihydrotestosteroneGV1001 peptidePeptide FragmentsReceptors, AndrogenTelomeraseandrogen receptorbenign prostate hyperplasiadihydrotestosteroneepithelia-mesenchymal transitionGV1001

Identifiers

PMID33539321
PMCPMC7906190
OpenAlexW3128907667

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.