RAC1 plays an essential role in estrogen receptor alpha function in breast cancer cells.


Journal

Oncogene
ISSN: 1476-5594
Titre abrégé: Oncogene
Pays: England
ID NLM: 8711562

Informations de publication

Date de publication:
10 2021
Historique:
received: 30 10 2020
accepted: 26 07 2021
revised: 14 07 2021
pubmed: 11 8 2021
medline: 27 1 2022
entrez: 10 8 2021
Statut: ppublish

Résumé

The activity of Rho family GTPase protein, RAC1, which plays important normal physiological functions, is dysregulated in multiple cancers. RAC1 is expressed in both estrogen receptor alpha (ER)-positive and ER-negative breast cancer (BC) cells. However, ER-positive BC is more sensitive to RAC1 inhibition. We have determined that reducing RAC1 activity, using siRNA or EHT 1864 (a small molecule Rac inhibitor), leads to rapid ER protein degradation. RAC1 interacts with ER within the ER complex and RAC1 localizes to chromatin binding sites for ER upon estrogen treatment. RAC1 activity is important for RNA Pol II function at both promoters and enhancers of ER target genes and ER-regulated gene transcription is blocked by EHT 1864, in a dose-dependent manner. Having identified that RAC1 is an essential ER cofactor for ER protein stability and ER transcriptional activity, we report that RAC1 inhibition could be an effective therapeutic approach for ER-positive BC.

Identifiants

pubmed: 34373577
doi: 10.1038/s41388-021-01985-1
pii: 10.1038/s41388-021-01985-1
pmc: PMC8497275
doi:

Substances chimiques

Estrogen Receptor alpha 0
RAC1 protein, human 0
rac1 GTP-Binding Protein EC 3.6.5.2

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

5950-5962

Subventions

Organisme : NCI NIH HHS
ID : P30 CA240139
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA166835
Pays : United States

Informations de copyright

© 2021. The Author(s).

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Auteurs

Jun Sun (J)

Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA.
Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA.

Gabriel Gaidosh (G)

Department of Human Genetics, University of Miami, Miami, FL, USA.

Ye Xu (Y)

Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA.
Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA.

Adnan Mookhtiar (A)

Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA.

Na Man (N)

Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA.

Pradeep Reddy Cingaram (PR)

Department of Human Genetics, University of Miami, Miami, FL, USA.

Ezra Blumenthal (E)

Department of Human Genetics, University of Miami, Miami, FL, USA.

Ramin Shiekhattar (R)

Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Department of Human Genetics, University of Miami, Miami, FL, USA.

Erik T Goka (ET)

Geneyus, LLC, Miami, FL, USA.

Stephen D Nimer (SD)

Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA. snimer@med.miami.edu.
Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA. snimer@med.miami.edu.
Department of Biochemistry and Molecular Biology, University of Miami, Miami, FL, USA. snimer@med.miami.edu.

Marc E Lippman (ME)

Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA. mlippman@med.miami.edu.
Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA. mlippman@med.miami.edu.

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