Evidence map›Paper›PMID 32146725›Full record

ArticleJournal of diabetes investigation2020

Activation of overexpressed glucagon-like peptide-1 receptor attenuates prostate cancer growth by inhibiting cell cycle progression.

Toru Shigeoka, Takashi Nomiyama, Takako Kawanami, Yuriko Hamaguchi, Tsuyoshi Horikawa, Tomoko Tanaka, Shinichiro Irie, Ryoko Motonaga, Nobuya Hamanoue, Makito Tanabe and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

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  14. The GLP-1 receptor is expressedEndocrine oncology (Bristol, England) · 2024
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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

14 authors at 2 institutions in 1 country.

Toru ShigeokaDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Takashi NomiyamaDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.ORCID https://orcid.org/0000-0001-7040-1334
Takako KawanamiDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Yuriko HamaguchiDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Tsuyoshi HorikawaDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Tomoko TanakaDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Shinichiro IrieDepartment of Urology, School of Medicine, Fukuoka University, Fukuoka, Japan.
Ryoko MotonagaDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Nobuya HamanoueDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Makito TanabeDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Kazuki NabeshimaDepartment of Pathology, School of Medicine, Fukuoka University, Fukuoka, Japan.
Masatoshi TanakaDepartment of Urology, School of Medicine, Fukuoka University, Fukuoka, Japan.
Toshihiko YanaseResearch institute for Islet Biology, Fukuoka University, Fukuoka, Japan.ORCID https://orcid.org/0000-0003-2971-9943
Daiji KawanamiDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.ORCID https://orcid.org/0000-0002-8926-4701
Fukuoka University · JPFukuoka Institute of Technology · JP

Funding

Astellas PharmaBoehringer IngelheimEli Lilly and CompanyMerck Sharp and DohmeMitsubishi Tanabe Pharma CorporationNovartisSanofiTakeda PharmaceuticalsThe Ministry of Education, Sports and Culture of Japan 18K08532
6 · The paper itself

Abstract

AIMS/

introductionIncretin therapy is a common treatment for type 2 diabetes mellitus. We have previously reported an anti-prostate cancer effect of glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4. The attenuation of cell proliferation in the prostate cancer cell line was dependent on GLP-1R expression. Here, we examined the relationship between human prostate cancer severity and GLP-1R expression, as well as the effect of forced expression of GLP-1R using a lentiviral vector. MATERIALS AND

methodsProstate cancer tissues were extracted by prostatectomy and biopsy. GLP-1R was overexpressed in ALVA-41 cells using a lentiviral vector (ALVA-41-GLP-1R cells). GLP-1R expression was detected by immunohistochemistry and quantitative polymerase chain reaction. Cell proliferation was examined by growth curves and bromodeoxyuridine incorporation assays. Cell cycle distribution and regulators were examined by flow cytometry and western blotting. In vivo experiments were carried out using a xenografted model.

resultsGLP-1R expression levels were significantly inversely associated with the Gleason score of human prostate cancer tissues. Abundant GLP-1R expression and functions were confirmed in ALVA-41-GLP-1R cells. Exendin-4 significantly decreased ALVA-41-GLP-1R cell proliferation in a dose-dependent manner. DNA synthesis and G1-to-S phase transition were inhibited in ALVA-41-GLP-1R cells. SKP2 expression was decreased and p27Kip1 protein was subsequently increased in ALVA-41-GLP-1R cells treated with exendin-4. In vivo experiments carried out by implanting ALVA-41-GLP-1R cells showed that exendin-4 decreased prostate cancer growth by activation of GLP-1R overexpressed in ALVA41-GLP-1R cells.

conclusionsForced expression of GLP-1R attenuates prostate cancer cell proliferation by inhibiting cell cycle progression in vitro and in vivo. Therefore, GLP-1R activation might be a potential therapy for prostate cancer.

Indexed as

Cell CycleGene Expression Regulation, NeoplasticAdultAgedAged, 80 and overAnimalsApoptosisBiomarkers, TumorCell ProliferationGlucagon-Like Peptide-1 ReceptorHumansMaleMiceMice, NudeMiddle AgedPrognosisBiomarkers, TumorGLP1R protein, humanGlucagon-Like Peptide-1 ReceptorCell cycleGlucagon-like peptide-1 receptorProstate cancer

Identifiers

PMID32146725
PMCPMC7477521
OpenAlexW3009314141

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.