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


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
18 06 2021
Historique:
received: 30 07 2020
accepted: 19 05 2021
entrez: 19 6 2021
pubmed: 20 6 2021
medline: 7 7 2021
Statut: epublish

Résumé

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.

Identifiants

pubmed: 34145268
doi: 10.1038/s41467-021-23974-4
pii: 10.1038/s41467-021-23974-4
pmc: PMC8213733
doi:

Substances chimiques

Antineoplastic Agents 0
Foxa1 protein, mouse 0
Hepatocyte Nuclear Factor 3-alpha 0
Nrf1 protein, mouse 0
Nuclear Respiratory Factor 1 0
Octamer Transcription Factor-3 0
Pou5f1 protein, mouse 0
Receptors, Androgen 0
Ribavirin 49717AWG6K

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3766

Commentaires et corrections

Type : CommentIn

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Auteurs

Ken-Ichi Takayama (KI)

Department of Systems Aging Science and Medicine, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.

Takeo Kosaka (T)

Department of Urology, Keio University School of Medicine, Tokyo, Japan.

Takashi Suzuki (T)

Department of Pathology and Histotechnology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.

Hiroshi Hongo (H)

Department of Urology, Keio University School of Medicine, Tokyo, Japan.

Mototsugu Oya (M)

Department of Urology, Keio University School of Medicine, Tokyo, Japan.

Tetsuya Fujimura (T)

Department of Urology, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Yutaka Suzuki (Y)

Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.

Satoshi Inoue (S)

Department of Systems Aging Science and Medicine, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. sinoue@tmig.or.jp.
Division of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan. sinoue@tmig.or.jp.

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