Evidence map›Paper›PMID 27561382›Full record

ArticleScientific reports2016

Dihydrotestosterone synthesis pathways from inactive androgen 5α-androstane-3β,17β-diol in prostate cancer cells: Inhibition of intratumoural 3β-hydroxysteroid dehydrogenase activities by abiraterone.

Takashi Ando, Tsutomu Nishiyama, Itsuhiro Takizawa, Fumio Ishizaki, Yoshimichi Miyashiro, Keisuke Takeda, Noboru Hara, Yoshihiko Tomita

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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  7. Simultaneous determination of dihydrotestosterone and its metabolites in mouse sera by LC-MS/MS with chemical derivatization.Journal of chromatography. B, Analytical technologies in the biomedical and life sciences · 2018
    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

8 authors at 2 institutions in 1 country.

Takashi AndoNiigata University Graduate School of Medical and Dental Sciences, Department of Regenerative and Transplant Medicine, Niigata, 951-8510, Japan.
Tsutomu NishiyamaNiigata University Graduate School of Medical and Dental Sciences, Department of Regenerative and Transplant Medicine, Niigata, 951-8510, Japan.
Itsuhiro TakizawaNiigata University Graduate School of Medical and Dental Sciences, Department of Regenerative and Transplant Medicine, Niigata, 951-8510, Japan.
Fumio IshizakiNiigata University Graduate School of Medical and Dental Sciences, Department of Regenerative and Transplant Medicine, Niigata, 951-8510, Japan.
Yoshimichi MiyashiroASKA Pharmaceutical medical Co. Ltd., Kawasaki, 213-8522, Japan.
Keisuke TakedaNiigata University Graduate School of Medical and Dental Sciences, Department of Regenerative and Transplant Medicine, Niigata, 951-8510, Japan.
Noboru HaraNiigata University Graduate School of Medical and Dental Sciences, Department of Regenerative and Transplant Medicine, Niigata, 951-8510, Japan.
Yoshihiko TomitaNiigata University Graduate School of Medical and Dental Sciences, Department of Regenerative and Transplant Medicine, Niigata, 951-8510, Japan.
Niigata University · JPASKA Pharmaceutical (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intratumoural dihydrotestosterone (DHT) synthesis could be an explanation for castration resistance in prostate cancer (PC). By using liquid chromatography-mass spectrometry, we evaluated the intratumoral DHT synthesis from 5α-androstane-3β,17β-diol (3β-diol), which is inactive androgen metabolized from DHT. 3β-diol had biochemical potential to be converted to DHT via three metabolic pathways and could stimulate PC cell growth. Especially, 3β-diol was not only converted back to upstream androgens such as dehydroepiandrosterone (DHEA) or Δ5-androstenediol but also converted directly to DHT which is the main pathway from 3β-diol to DHT. Abiraterone had a significant influence on the metabolism of DHEA, epiandrosterone and 3β-diol, by the inhibition of the intratumoural 3β-hydroxysteroid dehydrogenase (3β-HSD) activities which is one of key catalysts in androgen metabolic pathway. The direct-conversion of 3β-diol to DHT was catalysed by 3β-HSD and abiraterone could inhibit this activity of 3β-HSD. These results suggest that PC had a mechanism of intratumoural androgen metabolism to return inactive androgen to active androgen and intratumoural DHT synthesis from 3β-diol is important as one of the mechanisms of castration resistance in PC. Additionally, the inhibition of intratumoural 3β-HSD activity could be a new approach to castration-resistant prostate cancer treatment.

Indexed as

3-Hydroxysteroid DehydrogenasesAndrostane-3,17-diolAndrostenesCell Line, TumorDihydrotestosteroneEnzyme InhibitorsHumansMaleNeoplasm ProteinsProstatic Neoplasms3-Hydroxysteroid DehydrogenasesabirateroneAndrostane-3,17-diolAndrostenesDihydrotestosteroneEnzyme InhibitorsNeoplasm Proteins

Identifiers

PMID27561382
PMCPMC4999866
OpenAlexW2517095380

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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.