Neuroendocrine differentiation and the bombesin/gastrin‐releasing peptide family of neuropeptides in the progression of human prostate cancer

Aprikian, Armen; Han, Kehan; Laurent, Césari; Landry, France; Bégin, Louis R.; Chevalier, Simone

doi:10.1002/(sici)1097-0045(1998)8+<52::aid-pros9>3.3.co;2-j

Cited by 10 publications

(12 citation statements)

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“…In vivo growth of Ace-1-huGRPr subcutaneous tumors in bombesin (BBN)-treated and control mice. (A) Plot represents the tumor volume of subcutaneous xenografts at different time points (4,7,11,13,15,18, and 21 day). (B) Box and whisker represents the tumor weights in the two groups at the end of the study.…”

Section: Discussionmentioning

confidence: 99%

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Gastrin-releasing peptide receptor (GRPr) promotes EMT, growth, and invasion in canine prostate cancer

et al. 2016

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BACKGROUND The gastrin-releasing peptide receptor (GRPr) is upregulated in early and late-stage human prostate cancer (PCa) and other solid tumors of the mammary gland, lung, head and neck, colon, uterus, ovary, and kidney. However, little is known about its role in prostate cancer. This study examined the effects of a heterologous GRPr agonist, bombesin (BBN), on growth, motility, morphology, gene expression, and tumor phenotype of an osteoblastic canine prostate cancer cell line (Ace-1) in vitro and in vivo. METHODS The Ace-1 cells were stably transfected with the human GRPr and tumor cells were grown in vitro and as subcutaneous and intratibial tumors in nude mice. The effect of BBN was measured on cell proliferation, cell migration, tumor growth (using bioluminescence), tumor cell morphology, bone tumor phenotype, and epithelial-mesenchymal transition (EMT) and metastasis gene expression (quantitative RT-PCR). GRPr mRNA expression was measured in primary canine prostate cancers and normal prostate glands. RESULTS Bombesin (BBN) increased tumor cell proliferation and migration in vitro and tumor growth and invasion in vivo. BBN upregulated epithelial-to-mesenchymal transition (EMT) markers (TWIST, SNAIL, and SLUG mRNA) and downregulated epithelial markers (E-cadherin and β-catenin mRNA), and modified tumor cell morphology to a spindle cell phenotype. Blockade of GRPr upregulated E-cadherin and downregulated VIMENTIN and SNAIL mRNA. BBN altered the in vivo tumor phenotype in bone from an osteoblastic to osteolytic phenotype. Primary canine prostate cancers had increased GRPr mRNA expression compared to normal prostates. CONCLUSION These data demonstrated that the GRPr is important in prostate cancer growth and progression and targeting GRPr may be a promising strategy for treatment of prostate cancer.

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Section: Discussionmentioning

confidence: 99%

“…GRP has been shown to promote tumor growth and differentiation in multiple human cancers [17]. GRPr signaling promoted the development of androgen-independent prostate cancer [18,19], and activation of GRPr in the prostate resulted in upregulation of promoters of angiogenesis, which are essential for the development of metastasis [20].…”

Section: Introductionmentioning

confidence: 99%

Gastrin-releasing peptide receptor (GRPr) promotes EMT, growth, and invasion in canine prostate cancer

et al. 2016

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“…However, measuring serum levels of ProGRP enables us to understand the environment of GRP regulation in prostate cancer in vivo, and may provide information that compensates for the inadequacy of the current system of diagnosis using PSA. At present, studies on several cytotoxic antagonists targeting GRP receptor or tyrosine kinase inhibitor for the treatment of androgen-independent prostate cancer are underway; in addition, the combination of these antagonists and LH-RH analogue has been reported to inhibit tumor growth efficiently [33][34][35][36]. When these drugs become available for clinical practice, serum ProGRP may be useful as an indicator to monitor their use, suggesting the possibility of made-to-order therapy in the near future.…”

Section: Discussionmentioning

confidence: 99%

Elevated serum progastrin‐releasing peptide (31–98) in metastatic and androgen‐independent prostate cancer patients*

et al. 2002

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The clinical results demonstrated the existence of a regulatory mechanism for GRP, which to date had only been observed in cell lines. These findings suggest that GRP is a growth factor potentially upregulated by androgen but that does not rely principally on androgen modulation. The large overlap in levels of ProGRP among the groups limits the use of this value as a monitoring tool. Measurement of ProGRP, however, does have potential as an independent parameter to evaluate androgen-independent progression and to facilitate a new therapeutic strategy that may compensate for current limitations of diagnosis based on PSA alone.

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“…Bombesinlike peptides can stimulate the growth of PC-3 and DU-145 human androgen-independent prostate cancer cell lines [25] and promote the invasiveness of DU-145 cells in vitro [26]. Aprikian et al [27] proposed that the secretion of bombesin/GRP by neuroendocrine (NE) cells might be responsible for prostate cancer progression, androgen independence, and poor prognosis.…”

Section: Antagonists Of Bombesin/ Gastrin-releasing Peptide (Grp)mentioning

confidence: 99%

Peptide analogs in the therapy of prostate cancer

et al. 2000

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The use of peptide analogs in the therapy of prostate cancer is reviewed. The preferred primary treatment of advanced androgen‐dependent prostate cancer is presently based on the use of depot preparations of LH‐RH agonists. This treatment is likewise recommended in patients with rising PSA levels after surgery or radiotherapy. LH‐RH agonists with or without antiandrogens can be also utilized prior to or following various local treatments in patients with clinically localized prostate cancer and at high risk for disease recurrence. LH‐RH antagonists like Cetrorelix are in clinical trials. However, most patients with advanced prostatic carcinoma treated by any modality of androgen deprivation eventually relapse. Treatment of relapsed androgen‐independent prostate cancer remains a major challenge, but new therapeutic modalities are being developed based on antagonists of growth hormone‐releasing hormone (GH‐RH) and bombesin, which inhibit growth factors or their receptors. Another approach consists of cytotoxic analogs of LH‐RH, bombesin, and somatostatin containing doxorubicin or 2‐pyrrolinodoxorubicin, which can be targeted to receptors for these peptides found in prostate cancers and their metastases. These cytotoxic analogs inhibit growth of experimental androgen‐dependent or ‐independent prostate cancers and reduce the incidence of metastases. A rational therapy with peptide analogs could be selected on the basis of receptors present in biopsy samples. The approaches based on peptide analogs should result in a more effective treatment for prostate cancer. Prostate 45:158–166, 2000. © 2000 Wiley‐Liss, Inc.

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Neuroendocrine differentiation and the bombesin/gastrin‐releasing peptide family of neuropeptides in the progression of human prostate cancer

Cited by 10 publications

References 0 publications

Gastrin-releasing peptide receptor (GRPr) promotes EMT, growth, and invasion in canine prostate cancer

Gastrin-releasing peptide receptor (GRPr) promotes EMT, growth, and invasion in canine prostate cancer

Elevated serum progastrin‐releasing peptide (31–98) in metastatic and androgen‐independent prostate cancer patients*

Peptide analogs in the therapy of prostate cancer

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