Linked Life Data

11920625

Source:http://linkedlifedata.com/resource/pubmed/id/11920625

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-3-28
pubmed:abstractText
Vasoactive intestinal peptide (VIP) stimulates the proliferation and invasiveness of malignant prostatic cells. Receptors for VIP and the closely related growth hormone-releasing hormone (GH-RH) show considerable homology and are found in prostatic and other carcinomas. Among various analogs of GH-RH synthesized, JV-1-52 is a non-selective VIP/GH-RH antagonist, whereas JV-1-53 is a VIP antagonist devoid of GH-RH antagonistic effect. In our study, nude mice bearing PC-3 human androgen-independent prostate carcinomas were treated with JV-1-52 or JV-1-53 (20 microg/day, s.c.) for 28 days. Both antagonists produced a similar reduction in tumor volume (62-67%, p < 0.01) and tumor weight (59-62%; p < 0.05) vs. controls and extended tumor doubling-time from 9.1 to about 16 days (p < 0.05). To investigate the mechanisms involved, in another study we compared the effects of JV-1-53 with those of somatostatin analog RC-160. VIP antagonist JV-1-53 reduced tumor weight by 67% (p < 0.01) and suppressed the expression of mRNA for c-fos and c-jun oncogenes by about 34% (p < 0.05), without affecting serum levels of insulin-like growth factor-I (IGF-I). In contrast, RC-160 (50 microg/day) reduced serum IGF-I by 19% (p < 0.05), but did not significantly decrease tumor weight. mRNA for VIP and high affinity receptors for VIP were detected on PC-3 tumors. Our results suggest that VIP/GH-RH antagonists can inhibit the growth of androgen-independent prostate cancer by abrogating the autocrine/paracrine mitogenic stimuli of VIP. The ability of GH-RH antagonists to block tumoral VIP receptors, in addition to GH-RH receptors, could be potentially beneficial for prostate cancer therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
98
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
624-9
pubmed:dateRevised
2007-7-24
pubmed:meshHeading
pubmed-meshheading:11920625-Animals, pubmed-meshheading:11920625-Binding, Competitive, pubmed-meshheading:11920625-Cell Division, pubmed-meshheading:11920625-Growth Hormone-Releasing Hormone, pubmed-meshheading:11920625-Humans, pubmed-meshheading:11920625-Insulin-Like Growth Factor I, pubmed-meshheading:11920625-Male, pubmed-meshheading:11920625-Mice, pubmed-meshheading:11920625-Mice, Nude, pubmed-meshheading:11920625-Peptide Fragments, pubmed-meshheading:11920625-Prostatic Neoplasms, pubmed-meshheading:11920625-Proto-Oncogene Proteins c-fos, pubmed-meshheading:11920625-Proto-Oncogene Proteins c-jun, pubmed-meshheading:11920625-RNA, Messenger, pubmed-meshheading:11920625-Receptors, Vasoactive Intestinal Peptide, pubmed-meshheading:11920625-Time Factors, pubmed-meshheading:11920625-Tumor Cells, Cultured, pubmed-meshheading:11920625-Vasoactive Intestinal Peptide, pubmed-meshheading:11920625-Xenograft Model Antitumor Assays
pubmed:year
2002
pubmed:articleTitle
Inhibition of PC-3 human prostate cancers by analogs of growth hormone-releasing hormone (GH-RH) endowed with vasoactive intestinal peptide (VIP) antagonistic activity.
pubmed:affiliation
Endocrine, Polypeptide and Cancer Institute, Veterans Affairs Medical Center, New Orleans, LA 70112-1262, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't