ONECUT2 is a druggable driver of luminal to basal breast cancer plasticity.

Breast cancer Cell plasticity Estrogen receptor Heterogeneity ONECUT2 Transcription factor

Journal

Cellular oncology (Dordrecht)
ISSN: 2211-3436
Titre abrégé: Cell Oncol (Dordr)
Pays: Netherlands
ID NLM: 101552938

Informations de publication

Date de publication:
31 May 2024
Historique:
accepted: 03 05 2024
medline: 31 5 2024
pubmed: 31 5 2024
entrez: 31 5 2024
Statut: aheadofprint

Résumé

Tumor heterogeneity complicates patient treatment and can be due to transitioning of cancer cells across phenotypic cell states. This process is associated with the acquisition of independence from an oncogenic driver, such as the estrogen receptor (ER) in breast cancer (BC), resulting in tumor progression, therapeutic failure and metastatic spread. The transcription factor ONECUT2 (OC2) has been shown to be a master regulator protein of metastatic castration-resistant prostate cancer (mCRPC) tumors that promotes lineage plasticity to a drug-resistant neuroendocrine (NEPC) phenotype. Here, we investigate the role of OC2 in the dynamic conversion between different molecular subtypes in BC. We analyze OC2 expression and clinical significance in BC using public databases and immunohistochemical staining. In vitro, we perform RNA-Seq, RT-qPCR and western-blot after OC2 enforced expression. We also assess cellular effects of OC2 silencing and inhibition with a drug-like small molecule in vitro and in vivo. OC2 is highly expressed in a substantial subset of hormone receptor negative human BC tumors and tamoxifen-resistant models, and is associated with poor clinical outcome, lymph node metastasis and heightened clinical stage. OC2 inhibits ER expression and activity, suppresses a gene expression program associated with luminal differentiation and activates a basal-like state at the gene expression level. We also show that OC2 is required for cell growth and survival in metastatic BC models and that it can be targeted with a small molecule inhibitor providing a novel therapeutic strategy for patients with OC2 active tumors. The transcription factor OC2 is a driver of BC heterogeneity and a potential drug target in distinct cell states within the breast tumors.

Identifiants

pubmed: 38819630
doi: 10.1007/s13402-024-00957-3
pii: 10.1007/s13402-024-00957-3
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s).

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Auteurs

Irene Zamora (I)

Department of Health Sciences, Public University of Navarre, Pamplona, Navarre, Spain.

Mirian Gutiérrez (M)

Department of Health Sciences, Public University of Navarre, Pamplona, Navarre, Spain.

Alex Pascual (A)

Department of Health Sciences, Public University of Navarre, Pamplona, Navarre, Spain.

María J Pajares (MJ)

Department of Health Sciences, Public University of Navarre, Pamplona, Navarre, Spain.
IdiSNA, Navarre Institute for Health Research, Pamplona, Navarre, Spain.

Miguel Barajas (M)

Department of Health Sciences, Public University of Navarre, Pamplona, Navarre, Spain.
IdiSNA, Navarre Institute for Health Research, Pamplona, Navarre, Spain.

Lillian M Perez (LM)

Department of Urology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Sungyong You (S)

Department of Urology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Beatrice S Knudsen (BS)

Department of Pathology, University of Utah, Salt Lake City, UT, USA.

Michael R Freeman (MR)

Department of Urology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.

Ignacio J Encío (IJ)

Department of Health Sciences, Public University of Navarre, Pamplona, Navarre, Spain.
IdiSNA, Navarre Institute for Health Research, Pamplona, Navarre, Spain.

Mirja Rotinen (M)

Department of Health Sciences, Public University of Navarre, Pamplona, Navarre, Spain. mirja.rotinen@unavarra.es.
IdiSNA, Navarre Institute for Health Research, Pamplona, Navarre, Spain. mirja.rotinen@unavarra.es.

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