Evidence map›Paper›PMID 31401673›Full record

ArticleJournal of cancer research and clinical oncology2019

Dihydrotestosterone promotes kidney cancer cell proliferation by activating the STAT5 pathway via androgen and glucocorticoid receptors.

Sahyun Pak, Wansuk Kim, Yunlim Kim, Cheryn Song, Hanjong Ahn

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  8. The influence of sex hormones on renal cell carcinoma.Therapeutic advances in medical oncology · 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

5 authors at 3 institutions in 1 country.

Sahyun Pak *Department of Urology, Center for Urologic Cancer, National Cancer Center, Goyang, Korea.
Wansuk Kim *Department of Urology, Inje University Busan Paik Hospital, Busan, Korea.
Yunlim KimAsan Institute for Life Science, Asan Medical Center, Seoul, Korea.
Cheryn SongDepartment of Urology, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea.
Hanjong AhnDepartment of Urology, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea. hjahn@amc.seoul.kr.ORCID http://orcid.org/0000-0001-7608-5352
Ulsan College · KRInje University Busan Paik Hospital · KRNational Cancer Center · KR

Funding

Asan Institute for Life Sciences, Asan Medical Center 2014-012
6 · The paper itself

Abstract

purposeAndrogen receptors (ARs) are expressed on a variety of cell types, and AR signaling plays an important role in tumor development and progression in several cancers. This in vitro study evaluated the effect of dihydrotestosterone (DHT) on the proliferation of renal cell carcinoma (RCC) cells in relation to AR status.

methodsSteroid hormone receptor expression was evaluated using RT-PCR and Western blotting. The effect of DHT on cell proliferation and STAT5 phosphorylation was evaluated in RCC cell lines (Caki-2, A498, and SN12C) and primary RCC cells using cell viability assays and Western blotting. ARs and glucocorticoid receptors (GRs) were knocked down with small interfering RNAs before assessing changes in cell proliferation and STAT5 activation.

resultsDHT treatment promoted cell proliferation and increased STAT5 phosphorylation regardless of AR status. The AR antagonist bicalutamide reduced kidney cancer cell proliferation, regardless of AR status. AR and GR knockdown blocked STAT5 activation and reduced cell proliferation in all RCC cell lines. In patient-derived primary cells, DHT enhanced cell proliferation and this effect was diminished by treatment with the AR antagonists bicalutamide and enzalutamide and the GR antagonist mifepristone.

conclusionDHT promotes cell proliferation through STAT5 activation in RCC cells, regardless of AR status. DHT appears to utilize the AR and GR pathways to activate STAT5, and the inhibition of AR and GR showed antitumor activity in RCC cells. These data suggest that targeting AR and GR may be a promising new approach to the treatment of RCC.

Indexed as

Androgen Receptor AntagonistsCarcinoma, Renal CellCell Line, TumorCell ProliferationDihydrotestosteroneGene Expression Regulation, NeoplasticHumansKidney NeoplasmsReceptors, AndrogenReceptors, GlucocorticoidSignal TransductionSTAT5 Transcription FactorTumor Suppressor ProteinsAndrogen Receptor AntagonistsDihydrotestosteroneReceptors, AndrogenReceptors, GlucocorticoidSTAT5A protein, humanSTAT5 Transcription FactorTumor Suppressor ProteinsAndrogen receptorGlucocorticoid receptorKidney neoplasmsSTAT5 transcription factor

Identifiers

PMID31401673
PMCPMC11810384
OpenAlexW2967105783

What OpenQuestion holds

Textmetadata
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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.