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Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1480-5. Epub 2006 Jan 23.

Pten deletion leads to the expansion of a prostatic stem/progenitor cell subpopulation and tumor initiation.

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1
Departments of Molecular and Medical Pharmacology and Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California-Los Angeles, 650 Charles E. Young Drive South, Los Angeles, CA 90095, USA.

Abstract

PTEN (phosphatase and tensin homolog deleted on chromosome 10) is a potent tumor suppressor gene frequently mutated in human prostate cancers. Deletion of Pten in a murine model of prostate cancer recapitulates the disease progression seen in humans. Using defined cell lineage markers, we demonstrate that PTEN negatively regulates p63-positive prostatic basal cell proliferation without blocking differentiation. Concomitant with basal cell proliferation is the expansion of a prostate stem/progenitor-like subpopulation as evidenced by the progressive increase of stem cell antigen-1 (Sca-1)- and BCL-2-positive cells. This observation provides strong evidence that basal cell proliferation can be an initiating event for precancerous lesions. Sca-1(+) and BCL-2(+) progenitors may serve as cancer-initiating cells in this model.

PMID:
16432235
PMCID:
PMC1345717
DOI:
10.1073/pnas.0510652103
[Indexed for MEDLINE]
Free PMC Article
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