Evidence map›Paper›PMID 34145268›Full record

ArticleNature communications2021

Subtype-specific collaborative transcription factor networks are promoted by OCT4 in the progression of prostate cancer.

Ken-Ichi Takayama, Takeo Kosaka, Takashi Suzuki, Hiroshi Hongo, Mototsugu Oya, Tetsuya Fujimura, Yutaka Suzuki, Satoshi Inoue

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 42 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Ken-Ichi TakayamaDepartment of Systems Aging Science and Medicine, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.ORCID http://orcid.org/0000-0002-2832-1434
Takeo KosakaDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.ORCID http://orcid.org/0000-0002-4371-4594
Takashi SuzukiDepartment of Pathology and Histotechnology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.ORCID http://orcid.org/0000-0003-0195-815X
Hiroshi HongoDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.
Mototsugu OyaDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.
Tetsuya FujimuraDepartment of Urology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Yutaka SuzukiDepartment of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.ORCID http://orcid.org/0000-0003-4852-1879
Satoshi InoueDepartment of Systems Aging Science and Medicine, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. sinoue@tmig.or.jp.ORCID http://orcid.org/0000-0003-1247-3844
Keio University · JPTokyo Metropolitan Institute of Gerontology · JPJichi Medical University · JPThe University of Tokyo · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interactive networks of transcription factors (TFs) have critical roles in epigenetic and gene regulation for cancer progression. It is required to clarify underlying mechanisms for transcriptional activation through concerted efforts of TFs. Here, we show the essential role of disease phase-specific TF collaboration changes in advanced prostate cancer (PC). Investigation of the transcriptome in castration-resistant PC (CRPC) revealed OCT4 as a key TF in the disease pathology. OCT4 confers epigenetic changes by promoting complex formation with FOXA1 and androgen receptor (AR), the central signals for the progression to CRPC. Meanwhile, OCT4 facilitates a distinctive complex formation with nuclear respiratory factor 1 (NRF1) to gain chemo-resistance in the absence of AR. Mechanistically, we reveal that OCT4 increases large droplet formations with AR/FOXA1 as well as NRF1 in vitro. Disruption of TF collaborations using a nucleoside analogue, ribavirin, inhibited treatment-resistant PC tumor growth. Thus, our findings highlight the formation of TF collaborations as a potent therapeutic target in advanced cancer.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationDisease Models, AnimalDrug Resistance, NeoplasmGene Expression RegulationGene Expression Regulation, NeoplasticHEK293 CellsHepatocyte Nuclear Factor 3-alphaHumansMaleMiceMice, Inbred BALB CMice, NudeNuclear Respiratory Factor 1Antineoplastic AgentsFoxa1 protein, mouseHepatocyte Nuclear Factor 3-alphaNrf1 protein, mouseNuclear Respiratory Factor 1Octamer Transcription Factor-3Pou5f1 protein, mouseReceptors, AndrogenRibavirin

Identifiers

PMID34145268
PMCPMC8213733
OpenAlexW3173037166

What OpenQuestion holds

Textmetadata
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.