Evidence map›Paper›PMID 26483416›Full record

ArticleMolecular and cellular biology2016

Estrogen Exhibits a Biphasic Effect on Prostate Tumor Growth through the Estrogen Receptor β-KLF5 Pathway.

Yuka Nakajima, Asami Osakabe, Tsuyoshi Waku, Takashi Suzuki, Kensuke Akaogi, Tetsuya Fujimura, Yukio Homma, Satoshi Inoue, Junn Yanagisawa

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  14. Hormesis in Health and Chronic Diseases.Trends in endocrinology and metabolism: TEM · 2019
    Review
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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

9 authors at 3 institutions in 1 country.

Yuka NakajimaLife Science Center of Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Japan Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Japan nakajima@tara.tsukuba.ac.jp.
Asami OsakabeGraduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Japan.
Tsuyoshi WakuGraduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan.
Takashi SuzukiDepartment of Pathology and Histotechnology, Graduate School of Medicine, Tohoku University, Sendai, Japan.
Kensuke AkaogiGraduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Japan.
Tetsuya FujimuraDepartment of Urology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Yukio HommaDepartment of Urology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Satoshi InoueDepartment of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan Department of Anti-Aging Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan Division of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.
Junn YanagisawaLife Science Center of Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Japan Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Japan.
The University of Tokyo · JPUniversity of Tsukuba · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogens are effective in the treatment of prostate cancer; however, the effects of estrogens on prostate cancer are enigmatic. In this study, we demonstrated that estrogen (17β-estradiol [E2]) has biphasic effects on prostate tumor growth. A lower dose of E2 increased tumor growth in mouse xenograft models using DU145 and PC-3 human prostate cancer cells, whereas a higher dose significantly decreased tumor growth. We found that anchorage-independent apoptosis in these cells was inhibited by E2 treatment. Similarly, in vivo angiogenesis was suppressed by E2. Interestingly, these effects of E2 were abolished by knockdown of either estrogen receptor β (ERβ) or Krüppel-like zinc finger transcription factor 5 (KLF5). Ιn addition, E2 suppressed KLF5-mediated transcription through ERβ, which inhibits proapoptotic FOXO1 and proangiogenic PDGFA expression. Furthermore, we revealed that a nonagonistic ER ligand GS-1405 inhibited FOXO1 and PDGFA expression through the ERβ-KLF5 pathway and regulated prostate tumor growth without ERβ transactivation. Therefore, these results suggest that E2 biphasically modulates prostate tumor formation by regulating KLF5-dependent transcription through ERβ and provide a new strategy for designing ER modulators, which will be able to regulate prostate cancer progression with minimal adverse effects due to ER transactivation.

Indexed as

AnimalsCell Line, TumorCell ProliferationEstradiolEstrogen Receptor alphaEstrogen Receptor betaEstrogensHumansKruppel-Like Transcription FactorsMaleMiceProstateProstatic NeoplasmsSignal TransductionEstradiolEstrogen Receptor alphaEstrogen Receptor betaEstrogensKLF5 protein, humanKlf5 protein, mouseKruppel-Like Transcription Factors

Identifiers

PMID26483416
PMCPMC4702593
OpenAlexW2207619919

What OpenQuestion holds

Textmetadata
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.