Original paperInhibition of growth of androgen-independent DU-145 prostate cancer in vivo by luteinising hormone-releasing hormone antagonist cetrorelix and bombesin antagonists RC-3940-II and RC-3950-II☆
References (36)
- et al.
The Leuprolide Study Group. Clinical study of leuprolide depot formulation in the treatment of advanced prostate cancer
J Urol
(1990) - et al.
Somatostatin analog RC-160 and bombesin/gastrin-releasing peptide antagonist RC-3095 inhibit the growth of androgen-independent DU-145 human prostate cancer line in nude mice
Cancer Lett
(1993) - et al.
LH-RH analogue carrying a cytotoxic radical is internalized by rat pituitary cells in vitro
Peptides
(1994) - et al.
Screening of prostate cancer—necessity or nonsense?
Eur J Cancer
(1993) - et al.
Prostate specific antigen levels and clinical response to low dose dexamethasone for hormone-refractory metastatic prostate carcinoma
Cancer
(1995) - et al.
Present status of agonistic and antagonistic analogs of LH-RH in the treatment of advanced prostate cancer
Biomed Pharmacother
(1990) - et al.
Somatostatin receptors in human prostate and prostate cancer
J Clin Endocrin Metab
(1995) - et al.
Isolation of a human prostate carcinoma cell line
Int J Cancer
(1978) - et al.
Interaction between epidermal growth factor-mediated autocrine regulation and linoleic acid-stimulated growth of a human prostate cancer cell line
Prostate
(1992) - et al.
Sustained release formulations of luteinizing hormone-releasing hormone antagonist SB-75 inhibit proliferation and enhance apoptotic cell death of human prostate carcinoma (PC-82) in male nude mice
Cancer Res
(1992)
Growth inhibition of estrogen independent MXT mouse mammary carcinomas in mice treated with an agonist or antagonist of LH-RH, an analog of Somatostatin, or a combination
Breast Cancer Treat Res
Treatment with luteinizing hormone-releasing hormone antagonist SB-75 decreases levels of epidermal growth factor receptor and its mRNA in OV-1063 human epithelial ovarian cancer xeongrafts in nude mice
Int J Oncol
Characterization of high-affinity receptors for bombesin/gastrin releasing peptide on the human prostate cancer cell lines PC-3 and DU-145: Internalization of receptor bound 125I-(Tyr4) bombesin by tumor cells
Prostate
Bombesin-like peptides can function as autocrine growth factors in human small-cell lung cancer cells
Nature
Inhibitory effect of bombesin receptor antagonist RC-3095 on the growth of human pancreatic cancer cells in vivo and in vitro
Cancer Res
Stimulation by bombesin and inhibition by bombesin/gastrin-releasing peptide antagonist RC-3095 of growth of human breast cancer cell lines
Cancer Res
New pseudononapeptide bombesin antagonists with C-terminal LeuΨ(CH2N)Tac-NH2 showing high binding affinity to bombesin/GRP receptors in CFPAC-1 human pancreatic cancer cells
Int J Oncol
Potent bombesin antagonists with C-terminal LeuΨ(CH2N)Tac-NH2 or its derivatives
Cited by (94)
Regulation of prostate cancer by hormone-responsive G protein-coupled receptors
2018, Pharmacology and TherapeuticsGonadotropin-releasing hormone receptors as molecular therapeutic targets in prostate cancer: Current options and emerging strategies
2013, Cancer Treatment ReviewsCitation Excerpt :So far, the most studied GnRH antagonist in terms of direct inhibition of prostate cancer cell growth is cetrorelix. This compound has widely been shown to inhibit the proliferation of castration resistant prostate cancer cells, both in vitro and in vivo in preclinical models.208,213–215 Cetrorelix was also reported to decrease the migration and invasiveness of androgen-independent DU145 prostate cancer cells and this effect was mediated by reduced secretion and enzymatic activity of uPA and increased levels of its inhibitor plasminogen activator inhibitor-1/2.208
Differential signaling of the GnRH receptor in pituitary gonadotrope cell lines and prostate cancer cell lines
2013, Molecular and Cellular EndocrinologyCitation Excerpt :The dogma is that GnRH agonists desensitize the pituitary and GnRH antagonists block endogenous GnRH activity, both leading to reduced serum testosterone levels known as “chemical castration”. However, several reports have demonstrated evidence of a direct effect of GnRH upon sex hormone-dependent tumors including prostate cancer cells (Bahk et al., 1998; Dondi et al., 1994, 1998; Emons et al., 1996, 1997, 1998; Jungwirth et al., 1997; Kraus et al., 2004, 2006; Limonta et al., 1992, 1993, 1999; Moretti et al., 1996; Qayum et al., 1990a,b; Wells et al., 2002). Binding sites, expression of GnRH and its receptor (GnRHR) and direct growth regulatory effects of GnRH in the above cancer cells have been reported (Bahk et al., 1998; Dondi et al., 1994, 1998; Emons et al., 1996, 1997, 1998; Jungwirth et al., 1997; Kraus et al., 2004, 2006; Limonta et al., 1992, 1993, 1999; Moretti et al., 1996; Qayum et al., 1990a,b; Wells et al., 2002).
LHRH-conjugated lytic peptides directly target prostate cancer cells
2011, Biochemical PharmacologyCitation Excerpt :Further, synthetic peptides were more active and less toxic than their naturally occurring counterparts [6,13]. For example, we have synthesized highly sequence-divergent analogs for each of the peptide classes and have found some of them to be more active and less toxic than their natural counterparts [17–20]. Therapies directed at preventing or limiting the tumor's transition to the more aggressive invasive and metastatic stages offer benefits different from those designed to kill prostate cancer cells.
Will GnRH antagonists improve prostate cancer treatment?
2009, Trends in Endocrinology and MetabolismCitation Excerpt :In a more long-term study with repeated administration of leuprolide or antagonist, it was found that tumour growth with the antagonist was indistinguishable from that in castrates, whereas growth started to escape from agonist suppression at approximately five months [28]. The reason for this escape is unknown because both GnRH agonists and antagonists have been shown to exert a direct and specific antiproliferative effect on androgen-independent prostate cancer cell lines [29–32]. In the clinical setting, the percentage of men maintaining castrate testosterone levels from days 29 to 84 was comparable in patients receiving agonist and antagonist treatment [33].
- ☆
Presented in part at the 91st Annual Meeting of the American Urological Association, Orlando, Florida, 4–9 May 1996.
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On leave from the Department of Urology, Salzburg General Hospital, Salzburg, A-5020, Austria.