Neuroendocrine cells in the normal, hyperplastic and neoplastic prostate

Noordzij, Marinus A.; Steenbrugge, G.J. van; Kwast, Theodorus H. van der; Schröder, Fritz H.

doi:10.1007/bf00296871

Cited by 49 publications

(30 citation statements)

References 90 publications

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“…Whether PROMININ-2 might be a marker of both normal and/or tumor initiating progenitor cells or is expressed by the putative intermediate "transit ampliWer" pool of cells with mixed immunophenotypic proWle (van Leenders et al 2000;Tran et al 2002;Schalken and van Leenders 2003;Tokar et al 2005) remains to be established. Likewise, the potential expression of PROMININ-2 by neuroendocrine cells being sparsely scattered between the basal and luminal layers (Noordzij et al 1995) needs to be investigated as well. Nevertheless, being a transmembrane protein, PROMI-NIN-2 might be a valuable tool for prospective isolation and characterization of cells located in the basal part of the adult human prostatic epithelium.…”

Section: Discussionmentioning

confidence: 99%

“…The former cells are considered to be the precursors of the latter ones (Aumüller 1991;Signoretti and Loda 2006). It is of note that a third, minor population of cells, the so-called neuroendocrine cells of neurogenic origin with unresolved physiological function, has also been described in the prostatic glandular epithelium (Noordzij et al 1995;Aumüller et al 1999).…”

Section: Expression Of Prominin-1 and Prominin-2 In The Murine Epididmentioning

confidence: 99%

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Robust expression of Prominin-2 all along the adult male reproductive system and urinary bladder

Jászai

Fargeas

Haase

et al. 2008

Histochem Cell Biol

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Although the male reproductive system seems to be enriched in transcripts encoding for both Prominin genes, little is known about their spatial distribution in distinct segments of this organ system. This is especially true for the less-characterized second Prominin paralogue, Prominin-2. The present study, therefore, mainly examines the expression of Prominin-2 in male mice and reveals the existence of some crucial diVerences in the tissue compartmentalization of the two Prominin paralogues in the testis, epididymis, seminal vesicle, prostate and urinary bladder. Our in situ hybridization analysis demonstrates that the major domains of overlapping expression between the two Prominin genes are those compartments that are derived ontogenetically from the epigonadal mesonephric tubules, i.e. ductuli eVerentes, or from the WolYan-tube/ductus mesonephricus, for instance the corpus epididymidis and vesicula seminalis. In contrast, the sinus urogenitalis derivative urinary bladder epithelium expresses exclusively Prominin-2, but not Prominin-1 (CD133). The testis expresses only Prominin-1, not Prominin-2. In human prostate, we Wnally demonstrate that the expression of Prominin-2 (transcript and protein) is highly enriched in cells located in the basal compartment of the glandular epithelium where only a minute population was recently reported to be Prominin-1 positive. Taken together our data indicate that, except for the gonad, Prominin-2 is widely and abundantly expressed along the epithelia of various segments of the adult male genitourinary tract.

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Section: Discussionmentioning

confidence: 99%

Section: Expression Of Prominin-1 and Prominin-2 In The Murine Epididmentioning

confidence: 99%

Robust expression of Prominin-2 all along the adult male reproductive system and urinary bladder

Jászai

Fargeas

Haase

et al. 2008

Histochem Cell Biol

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“…Neuroendocrine (NE) cells are present in the normal and neoplastic prostate (1). Increases in NE phenotype and secretory products are closely correlated with tumor progression and androgen independence in prostate cancer (2,3).…”

Section: Introductionmentioning

confidence: 99%

NE-10 Neuroendocrine Cancer Promotes the LNCaP Xenograft Growth in Castrated Mice

et al. 2004

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Increases in neuroendocrine (NE) cells and their secretory products are closely correlated with tumor progression and androgen-independent prostate cancer. However, the mechanisms by which NE cells influence prostate cancer growth and progression, especially after androgen ablation therapy, are poorly understood. To investigate the role of NE cells on prostate cancer growth, LNCaP xenograft tumors were implanted into nude mice. After the LNCaP tumors were established, the NE mouse prostate allograft (NE-10) was implanted on the opposite flank of these nude mice to test whether NE tumor-derived systemic factors can influence LNCaP growth. Mice bearing LNCaP tumors with or without NE allografts were castrated 2 weeks after NE tumor inoculation, and changes in LNCaP tumor growth rate and gene expression were investigated. After castration, LNCaP tumor growth decreased in mice bearing LNCaP tumors alone, and this was accompanied by a loss of nuclear androgen receptor (AR) localization. In contrast, in castrated mice bearing both LNCaP and NE-10 tumors, LNCaP tumors continued to grow, had increased levels of nuclear AR, and secreted prostate-specific antigen. Therefore, in the absence of testicular androgens, NE secretions were sufficient to maintain LNCaP cell growth and androgen-regulated gene expression in vivo. Furthermore, in vitro experiments showed that NE secretions combined with low levels of androgens activated the AR, an effect that was blocked by the antiandrogen bicalutamide. Because an increase in AR level has been reported to be sufficient to account for hormone refractory prostate cancers, the NE cell population ability to increase AR level/activity can be another mechanism that allows prostate cancer to escape androgen ablation therapy.

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“…162,163 Neuroendocrine cells can be found in normal, hyperplastic and neoplastic prostatic tissues. Adenocarcinomas of the prostate which express neuroendocrine properties do not respond to androgen ablation therapy.…”

Section: Neuropeptidesmentioning

confidence: 99%

“…In addition, some of the neuropeptides secreted by the neuroendocrine cells may act as growth factors by activation of membrane receptors in an autocrine-paracrine fashion, or by ligand-independent activation of the androgen receptor in neighbouring non-neuroendocrine cells. 163 Elevated levels of neuropeptides and neuroendocrine markers in the serum of patients have been associated with poorer survival. 165 Androgen-independent cells have been reported to express bombesin, neurotensin and endothelin-1 receptors, 162,166,167 and receptor antagonists for the neuropeptides have been shown to inhibit the growth of prostate tumour xenografts.…”

Section: Neuropeptidesmentioning

confidence: 99%

Molecular and cellular biology of prostate cancer—the role of apoptosis as a target for therapy

Costa-Pereira

Cotter

1999

Prostate Cancer Prostatic Dis

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Despite the high incidence and mortality rate of prostate cancer, the molecular mechanisms underlying the progression of the disease remain to be fully elucidated. This paper reviews the current state of knowledge on prostatic carcinogenesis, focusing not only on the molecular genetics of prostate cancer, but also on the role of oncogenes, tumour suppressor genes, and growth factors. The remarkable ability of prostate cancer cells to survive androgen withdrawal and apoptosis are discussed, with particular emphasis on how apoptosis may be manipulated from a therapeutic viewpoint.

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Neuroendocrine cells in the normal, hyperplastic and neoplastic prostate

Cited by 49 publications

References 90 publications

Robust expression of Prominin-2 all along the adult male reproductive system and urinary bladder

Robust expression of Prominin-2 all along the adult male reproductive system and urinary bladder

NE-10 Neuroendocrine Cancer Promotes the LNCaP Xenograft Growth in Castrated Mice

Molecular and cellular biology of prostate cancer—the role of apoptosis as a target for therapy

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