Evidence map›Paper›PMID 30883989›Full record

ArticleCell proliferation2019

5-ARI induces autophagy of prostate epithelial cells through suppressing IGF-1 expression in prostate fibroblasts.

Bo-Yu Yang, Chen-Yi Jiang, Chen-Yun Dai, Rui-Zhe Zhao, Xing-Jie Wang, Yi-Ping Zhu, Yu-Xin Qian, Fu-Li Yin, Xiang-Yu Fu, Yi-Feng Jing and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

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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

13 authors at 2 institutions in 1 country.

Bo-Yu YangDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0002-0222-8071
Chen-Yi JiangDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chen-Yun DaiInstitute of Translational Medicine, Shanghai General Hospital, Shanghai, China.
Rui-Zhe ZhaoDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xing-Jie WangDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yi-Ping ZhuDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yu-Xin QianDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fu-Li YinDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiang-Yu FuDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yi-Feng JingDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Bang-Min HanDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0001-9101-8377
Shu-Jie XiaDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuan RuanDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0001-7580-0676
Shanghai Jiao Tong University · CNShanghai FRP Research Institute (China) · CN

Funding

National Natural Science Foundation of China 81300625National Natural Science Foundation of China 81502223National Natural Science Foundation of China 8157040171
6 · The paper itself

Abstract

objectives5α-reductase inhibitor (5-ARI) is a commonly used medicine in the treatment of lower urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH). Our study mainly focuses on the mechanism of BPH development after 5ARI treatment. MATERIALS AND

methodsProstate specimens from patients were collected. Insulin-like growth factor 1 (IGF-1), Beclin-1, LC3 levels, was analysed by immunohistochemistry. The role IGF-1 on autophagic flux in prostate epithelial cells was studied. Additionally, effect of autophagy on recombinant grafts consisting of prostate stromal and epithelial cells in nude mice was investigated.

resultsWe demonstrated that IGF-1 expression is down-regulated in prostate fibroblasts after long-term 5-ARI application. A decrease in IGF-1 levels was found to activate autophagic flux through the mTOR pathway in prostate epithelial cells, while the inhibition of IGF-1 receptor function induced autophagy in prostate epithelial cells. In addition, we revealed that blocking autophagic flux initiation can reduce the volume of recombinant grafts in vivo. Finally, our findings suggest that long-term 5-ARI application reduces IGF-1 secretion by prostatic stromal cells, thereby inducing autophagy of prostatic epithelial cells, which is one of the mechanisms underlying BPH pathogenesis and progression.

conclusionsFocusing on the autophagy induced by low levels of IGF-1 in prostatic epithelial cells, after elucidating AR signalling impairment of prostate stromal cells, might provide a novel strategy for the treatment and prevention of BPH development.

Indexed as

5-alpha Reductase InhibitorsAnimalsAutophagyBeclin-1Cells, CulturedDown-RegulationEpithelial CellsFibroblastsHeterograftsHumansInsulin-Like Growth Factor IMaleMiceMice, NudeMicrotubule-Associated ProteinsProstate5-alpha Reductase InhibitorsAR protein, humanBeclin-1BECN1 protein, humanIGF1 protein, humanInsulin-Like Growth Factor IMAP1LC3A protein, humanMicrotubule-Associated ProteinsMTOR protein, humanReceptors, AndrogenTOR Serine-Threonine Kinasesandrogen receptorbenign prostatic hyperplasiainsulin-like growth factor 1prostate epithelial cellsprostate fibroblasts

Identifiers

PMID30883989
PMCPMC6536403
OpenAlexW2924365008

What OpenQuestion holds

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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.