AR-V7 exhibits non-canonical mechanisms of nuclear import and chromatin engagement in castrate-resistant prostate cancer.


Journal

eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614

Informations de publication

Date de publication:
18 07 2022
Historique:
received: 27 08 2021
accepted: 17 07 2022
pubmed: 19 7 2022
medline: 26 8 2022
entrez: 18 7 2022
Statut: epublish

Résumé

Expression of the AR splice variant, androgen receptor variant 7 (AR-V7), in prostate cancer is correlated with poor patient survival and resistance to AR targeted therapies and taxanes. Currently, there is no specific inhibitor of AR-V7, while the molecular mechanisms regulating its biological function are not well elucidated. Here, we report that AR-V7 has unique biological features that functionally differentiate it from canonical AR-fl or from the second most prevalent variant, AR-v567. First, AR-V7 exhibits fast nuclear import kinetics via a pathway distinct from the nuclear localization signal dependent importin-α/β pathway used by AR-fl and AR-v567. We also show that the dimerization box domain, known to mediate AR dimerization and transactivation, is required for AR-V7 nuclear import but not for AR-fl. Once in the nucleus, AR-V7 is transcriptionally active, yet exhibits unusually high intranuclear mobility and transient chromatin interactions, unlike the stable chromatin association of liganded AR-fl. The high intranuclear mobility of AR-V7 together with its high transcriptional output, suggest a Hit-and-Run mode of transcription. Our findings reveal unique mechanisms regulating AR-V7 activity, offering the opportunity to develop selective therapeutic interventions.

Identifiants

pubmed: 35848798
doi: 10.7554/eLife.73396
pii: 73396
pmc: PMC9398446
doi:
pii:

Substances chimiques

AR protein, human 0
Chromatin 0
Protein Isoforms 0
Receptors, Androgen 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NCI NIH HHS
ID : R01 CA179100
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA062948
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA216800
Pays : United States
Organisme : NCI NIH HHS
ID : F32 CA220988
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA228512
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA203702
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA137020
Pays : United States

Informations de copyright

© 2022, Kim, Au, Jamalruddin et al.

Déclaration de conflit d'intérêts

SK, CA, MJ, NA, EM, LP, AB, DW, PV, DR, DN, PG No competing interests declared

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Auteurs

Seaho Kim (S)

Department of Medicine, Weill Cornell Medical College, New York, United States.

CheukMan C Au (CC)

Department of Medicine, Weill Cornell Medical College, New York, United States.

Mohd Azrin Bin Jamalruddin (MAB)

Department of Medicine, Weill Cornell Medical College, New York, United States.

Naira Essam Abou-Ghali (NE)

Department of Medicine, Weill Cornell Medical College, New York, United States.

Eiman Mukhtar (E)

Department of Medicine, Weill Cornell Medical College, New York, United States.

Luigi Portella (L)

Department of Medicine, Weill Cornell Medical College, New York, United States.

Adeline Berger (A)

Department of Pathology, Weill Cornell Medical College, New York, United States.

Daniel Worroll (D)

Department of Medicine, Weill Cornell Medical College, New York, United States.

Prerna Vatsa (P)

Department of Medicine, Weill Cornell Medical College, New York, United States.

David S Rickman (DS)

Department of Pathology, Weill Cornell Medical College, New York, United States.

David M Nanus (DM)

Department of Medicine, Weill Cornell Medical College, New York, United States.
Meyer Cancer Center, Weill Cornell Medical College, New York, United States.

Paraskevi Giannakakou (P)

Department of Medicine, Weill Cornell Medical College, New York, United States.
Meyer Cancer Center, Weill Cornell Medical College, New York, United States.

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