Evidence map›Paper›PMID 27270436›Full record

ArticleOncogene2016

Targeting Oct1 genomic function inhibits androgen receptor signaling and castration-resistant prostate cancer growth.

D Obinata, K Takayama, K Fujiwara, T Suzuki, S Tsutsumi, N Fukuda, H Nagase, T Fujimura, T Urano, Y Homma and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  15. Collective invasion of glioma cells through OCT1 signalling and interaction with reactive astrocytes after surgery.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Article
  16. Article
  17. Review
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  19. Article
  20. Metformin Targets Mitochondrial Glycerophosphate Dehydrogenase to Control Rate of Oxidative Phosphorylation and Growth of Thyroid CancerClinical cancer research : an official journal of the American Association for Cancer Research · 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

13 authors at 5 institutions in 1 country.

D ObinataDepartment of Anti-Aging Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
K TakayamaDepartment of Anti-Aging Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
K FujiwaraDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
T SuzukiDepartment of Pathology, Tohoku University Graduate School of Medicine, Miyagi, Japan.
S TsutsumiGenome Science Division, Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, Tokyo, Japan.
N FukudaDivision of Nephrology Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
H NagaseLaboratory of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba, Japan.
T FujimuraDepartment of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
T UranoDepartment of Anti-Aging Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Y HommaDepartment of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
H AburataniGenome Science Division, Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, Tokyo, Japan.
S TakahashiDepartment of Urology, Nihon University School of Medicine, Tokyo, Japan.
S InoueDepartment of Anti-Aging Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPNihon University · JPTokyo Metropolitan Institute of Gerontology · JPChiba Cancer Center · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Androgen receptor (AR) functions as a ligand-dependent transcription factor to regulate its downstream signaling for prostate cancer progression. AR complex formation by multiple transcription factors is important for enhancer activity and transcriptional regulation. However, the significance of such collaborative transcription factors has not been fully understood. In this study, we show that Oct1, an AR collaborative factor, coordinates genome-wide AR signaling for prostate cancer growth. Using global analysis by chromatin immunoprecipitation sequencing (ChIP-seq), we found that Oct1 is recruited to AR-binding enhancer/promoter regions and facilitates androgen signaling. Moreover, a major target of AR/Oct1 complex, acyl-CoA synthetase 3 (ACSL3), contributes to tumor growth in nude mice, and its high expression is associated with poor prognosis in prostate cancer patients. Next, we examined the therapeutic effects of pyrrole-imidazole polyamides that target the Oct1-binding sequence identified in the center of the ACSL3 AR-binding site. We observed that treatment with Oct1 polyamide severely blocked the Oct1 binding at the ACSL3 enhancer responsible for its transcriptional activity and ACSL3 induction. In addition, Oct1 polyamides suppressed castration-resistant tumor growth and specifically repressed global Oct1 chromatin association and androgen signaling in prostate cancer cells, with few nonspecific effects on basal promoter activity. Thus, targeting Oct1 binding could be a novel therapeutic strategy for AR-activated castration-resistant prostate cancer.

Indexed as

Androgen Receptor AntagonistsAnimalsCell Line, TumorCell ProliferationCoenzyme A LigasesGenomicsHumansImidazolesLong-Chain-Fatty-Acid-CoA LigaseMaleMiceMice, NudeMolecular Targeted TherapyNylonsOctamer Transcription Factor-1Prostatic Neoplasms, Castration-ResistantAndrogen Receptor AntagonistsAR protein, humanCoenzyme A LigasesImidazolesLong-Chain-Fatty-Acid-CoA LigaseNylonsOctamer Transcription Factor-1POU2F1 protein, humanPyrrolesReceptors, Androgen

Identifiers

PMID27270436
OpenAlexW2411692156

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.