Cited by 201Prostate Cancer Treatment and ResearchFibroblast Growth Factor ResearchProstate Cancer Diagnosis and Treatment

Enhanced Paracrine FGF10 Expression Promotes Formation of Multifocal Prostate Adenocarcinoma and an Increase in Epithelial Androgen Receptor

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Memarzadeh, Sanaz, Xin, Li, Mulholland, David J., Mansukhani, Alka, Wu, Hong, Teitell, Michael A., Witte, Owen N.·2007·Cancer Cell

Abstract

Enhanced mesenchymal expression of FGF10 led to the formation of multifocal PIN or prostate cancer. Inhibition of epithelial FGFR1 signaling using DN FGFR1 led to reversal of the cancer phenotype. A subset of the FGF10-induced carcinoma was serially transplantable. Paracrine FGF10 led to an increase in epithelial androgen receptor and synergized with cell-autonomous activated AKT. Our observations indicate that stromal FGF10 expression may facilitate the multifocal histology observed in prostate adenocarcinoma and suggest the FGF10/FGFR1 axis as a potential therapeutic target in treating hormone-sensitive or refractory prostate cancer. We also show that transient exposure to a paracrine growth factor may be sufficient for the initiation of oncogenic transformation.

Integrity signals

Registry

Crossref · 10.1016/j.ccr.2007.11.002

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59 of 59 references verified0 citation errors · 0 not checkable

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  • Expression of FGF10 by urogenital mesenchymal cells results in the induction of multifocal prostatic adenocarcinoma in epithelial cells.

    “For example, expression of fibroblast growth factor 10 (FGF10) by urogenital mesenchymal cells results in the induction of multifocal prostatic adenocarcinoma in epithelial cells.52”

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Authors
Memarzadeh, S., Xin, L., Mulholland, D. J., Mansukhani, A., Wu, H., Teitell, M. A., & Witte, O. N.
Affiliations
  • University of California, Los Angeles (US)
  • NYU Langone Health (US)
  • Howard Hughes Medical Institute (US)
Corresponding author
Witte, Owen N.
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2007-12
Volume
12
Issue
6
Pages
572-585
ISSN
1535-6108 (ISSN-L)
OpenAlex
W2011566841
Cited by
201
References
62
Citations by year
2025: 5 · 2024: 10 · 2023: 8 · 2022: 3 · 2021: 10 · 2020: 7 · 2019: 7 · 2018: 11 · 2017: 8 · 2016: 7 · 2015: 20 · 2014: 17 · 2013: 22 · 2012: 9
FWCI
11.97
Type
journal article
Language
en
Open access
Locations
  • Cancer Cell (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Howard Hughes Medical Institute
  • National Cancer Institute (R01CA107300, K12CA076905, K12-CA076905-09, R01CA107166, R01CA090571, K99CA125937)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (5K12HD00849-18, K12HD000849)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Diagnosis and Treatment
Keywords
FGF10, FGFR1, prostate adenocarcinoma, multifocal prostate cancer, paracrine signaling, mesenchymal stroma, androgen receptor, Akt activation, prostatic intraepithelial neoplasia, oncogenic transformation, hormone-sensitive prostate cancer, therapeutic target
MeSH terms
Animals, Cell Differentiation, Cell Survival, Cell Transformation, Neoplastic, Enzyme Activation, Epithelial Cells, Epithelium, Genes, Dominant, Male, Mesoderm, Neoplasm Transplantation, Organ Specificity, Prostatic Neoplasms, Receptors, Androgen, Regeneration, Prostatic Intraepithelial Neoplasia, Paracrine Communication, Cell Proliferation, Proto-Oncogene Proteins c-akt, Mice, Receptor, Fibroblast Growth Factor, Type 1, Fibroblast Growth Factor 10

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