Cell proliferation studies in the rat prostate: II. The effects of castration and androgen‐induced regeneration upon basal and secretory cell proliferation

Evans, Gareth S; Chandler, John

doi:10.1002/pros.2990110406

Cited by 151 publications

(105 citation statements)

References 27 publications

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“…Involution of the prostate gland following castration is associated with increased programmed cell death of luminal cells resulting in an approximately 80% loss of prostatic epithelial cells (Coffey et al 1968, Isaacs et al 1992. The glandular atrophy is incomplete, however, and histological findings in this and previous studies indicate that rudimentary glandular structures remain even after prolonged periods of castration (Sinha et al 1981, Evans & Chandler 1987a. These glandular rudiments consist of both luminal and basal cells, with a decreased relative proportion of luminal:basal cells (3:1 as compared with 13:1 in the intact animal).…”

Section: Discussionsupporting

confidence: 45%

“…The luminal cells have been reported as the differentiated progeny of basal progenitor cells of the prostate . However, the findings that not all luminal cells die during prostatic involution induced by androgen withdrawal (Sinha et al 1981, Sinha & Bentley 1984, English et al 1987, Evans & Chandler 1987a and that luminal cells proliferate rapidly following re-administration of testosterone (Sinha & Bentley 1984, English et al 1987, Evans & Chandler 1987a, have led to an alternative proposal of cellular hierarchies within the prostate. This model ascribes two separate cell lineages within the prostatic epithelium, a basal cell and luminal cell lineage, each with its own subpopulation of stem cells (Evans & Chandler 1987a,b).…”

Section: Introductionmentioning

confidence: 99%

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Androgen receptor expression of proliferating basal and luminal cells in adult murine ventral prostate

Mirosevich

Bentel²,

Zeps³

et al. 1999

Journal of Endocrinology

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Maintenance of the size and differentiated function of the adult prostate is dependent on testicular androgens. In this study, simultaneous androgen receptor (AR) immunohistochemistry and [3 H]thymidine labelling was used to characterise the proliferating epithelial cells of the murine ventral prostate. Proliferation in the adult prostate was more prevalent in the basal cell population with 1·8% AR-negative cells labelled with [3 H]thymidine as compared with 0·7% AR-expressing luminal cells. Three weeks following castration of mice, the atrophied prostate contained rudimentary glands composed of both luminal and basal cells with the proportion of AR-expressing basal cells reduced from 50 to 25%. Administration of testosterone enanthate to castrated mice induced a recapitulation of the prostate gland that was preceded by up-regulation of AR expression in basal cells to normal adult levels (50% AR-positive cells) by 12 h following testosterone injection. Proliferation of AR-positive luminal cells peaked at 48 h (22·8%) while proliferation of AR-negative basal cells peaked at 96 h (6·1%) following testosterone administration. These results suggest that distinct populations of luminal and basal cells are resistant to castration-induced involution of the prostate but remain responsive to direct or indirect testosterone effects and recapitulate the gland following administration of testosterone.

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Section: Discussionsupporting

confidence: 45%

Section: Introductionmentioning

confidence: 99%

Androgen receptor expression of proliferating basal and luminal cells in adult murine ventral prostate

Mirosevich

Bentel²,

Zeps³

et al. 1999

Journal of Endocrinology

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“…1B). This model is supported by observations that after castration, residual quiescent luminal cells remain in the rodent prostate that have high proliferative activity upon androgen add-back (Evans and Chandler 1987;Tsujimura et al 2002). Immunohistochemical (IHC) studies have also shown that fetal and prepubertal human epithelia appear positive for all cytokeratins, and no intermediate phenotype was seen in situ (Wernert et al 1987;Wang et al 2001).…”

Section: The Prostate Gland and Adult Prostate Stem Cellsmentioning

confidence: 87%

Epithelial Stem Cells of the Prostate and Their Role in Cancer Progression

Lukacs¹,

Lawson²,

Long-zuo³

et al. 2008

Cold Spring Harbor Symposia on Quantitative Biology

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Prostate cancer is a leading cause of cancer-related death in adult men. It can regress dramatically upon antihormonal therapy, but it often recurs in a more aggressive, androgen-independent form. Defining the prostate tissue stem cells (PrSCs) and their involvement in cancer initiation and maintenance may lead to better therapeutics. Using a tissue-regeneration model in which dissociated prostate epithelial cells mixed with inductive mesenchyme give rise to prostatic tubules, we have identified a small population of prostate cells that contains multiple stem cell characteristics. In this system, prostate cancer can be initiated by autocrine or paracrine growth factor signaling and intracellular overexpression of genes often found mutated in human prostate cancer. Using an in vitro prostate sphere assay, we further defined the PrSC population and demonstrated their selfrenewal and multilineage differentiation capabilities. Microarray analyses of the stem-and non-stem-cell populations have assisted us in finding and evaluating additional markers that can better define the PrSC population and further delineate the different cell types of the prostate, including those that serve as the target cell for tumor initiation.

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“…Following androgen ablation, 90% of the luminal cells, but only a small percentage of basal cells will undergo apoptosis during the process of regression (English et al, 1987;Evans and Chandler, 1987). Consequently, early studies favored a basal localization of stem cells, as most basal cells are castration resistant.…”

Section: Identification Of Normal Prostate Epithelial Stem Cells In Micementioning

confidence: 99%

Revisiting the concept of cancer stem cells in prostate cancer

Wang

Shen

2010

Oncogene

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The cancer stem cell (CSC) model proposes that cells within a tumor are organized in a hierarchical lineage relationship and display different tumorigenic potential, suggesting that effective therapeutics should target rare CSCs that sustain tumor malignancy. Here we review the current status of studies to identify CSCs in human prostate cancer as well as mouse models, with an emphasis on discussing different functional assays and their advantages and limitations. We also describe current controversies regarding the identification of prostate epithelial stem cells and cell types of origin for prostate cancer, and present potential resolutions of these issues. Although definitive evidence for the existence of CSCs in prostate cancer is still lacking, future directions pursuing the identification of tumor-initiating stem cells in the mouse may provide important advances in evaluating the CSC model for prostate cancer.

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Cell proliferation studies in the rat prostate: II. The effects of castration and androgen‐induced regeneration upon basal and secretory cell proliferation

Cited by 151 publications

References 27 publications

Androgen receptor expression of proliferating basal and luminal cells in adult murine ventral prostate

Androgen receptor expression of proliferating basal and luminal cells in adult murine ventral prostate

Epithelial Stem Cells of the Prostate and Their Role in Cancer Progression

Revisiting the concept of cancer stem cells in prostate cancer

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