Stromal androgen signaling acts as tumor niches to drive prostatic basal epithelial progenitor-initiated oncogenesis.


Journal

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

Informations de publication

Date de publication:
02 11 2022
Historique:
received: 27 05 2022
accepted: 19 10 2022
entrez: 3 11 2022
pubmed: 4 11 2022
medline: 5 11 2022
Statut: epublish

Résumé

The androgen receptor (AR)-signaling pathways are essential for prostate tumorigenesis. Although significant effort has been devoted to directly targeting AR-expressing tumor cells, these therapies failed in most prostate cancer patients. Here, we demonstrate that loss of AR in stromal sonic-hedgehog Gli1-lineage cells diminishes prostate epithelial oncogenesis and tumor development using in vivo assays and mouse models. Single-cell RNA sequencing and other analyses identified a robust increase of insulin-like growth factor (IGF) binding protein 3 expression in AR-deficient stroma through attenuation of AR suppression on Sp1-regulated transcription, which further inhibits IGF1-induced Wnt/β-catenin activation in adjacent basal epithelial cells and represses their oncogenic growth and tumor development. Epithelial organoids from stromal AR-deficient mice can regain IGF1-induced oncogenic growth. Loss of human prostate tumor basal cell signatures reveals in basal cells of stromal AR-deficient mice. These data demonstrate a distinct mechanism for prostate tumorigenesis and implicate co-targeting stromal and epithelial AR-signaling for prostate cancer.

Identifiants

pubmed: 36323713
doi: 10.1038/s41467-022-34282-w
pii: 10.1038/s41467-022-34282-w
pmc: PMC9630272
doi:

Substances chimiques

Androgens 0
Receptors, Androgen 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

6552

Subventions

Organisme : NCI NIH HHS
ID : R01 CA070297
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA166894
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK104941
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA233664
Pays : United States

Informations de copyright

© 2022. The Author(s).

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Auteurs

Alex Hiroto (A)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Won Kyung Kim (WK)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Ariana Pineda (A)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Yongfeng He (Y)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Dong-Hoon Lee (DH)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Vien Le (V)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Adam W Olson (AW)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Joseph Aldahl (J)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Christian H Nenninger (CH)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Alyssa J Buckley (AJ)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.

Guang-Qian Xiao (GQ)

Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Joseph Geradts (J)

Department of Pathology and Laboratory Medicine, Brody School of Medicine, East Carolina University, Greenville, NC, USA.

Zijie Sun (Z)

Department of Cancer Biology, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA. zjsun@coh.org.

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Classifications MeSH