Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-6-9
pubmed:abstractText
Cholecystokinin (CCK) is a gut-brain peptide has been described to be able to induce mitosis according to recent studies. Additionally, conflicting data has been published on whether tumours of the central and peripheral nervous system in general, and gliomas in particular, express CCK receptors. In the present in vitro study we employed reverse transcription followed by the polymerase chain reaction (RT-PCR) to investigate whether mRNA for CCK-A and CCK-B receptors as well as CCK peptide itself is present in primary human gliomas and the U-87 MG GBM cell line. The data show that 14/14 (100%) of the primary gliomas exhibited mRNA expression for the CCK peptide gene and the B receptor including the U-87 MG cells, whereas, only 2/14 (14%) showed presence of the CCK-A receptor. The presence of CCK receptors together with CCK peptide expression itself suggests presence of an autocrine loop controlling glioma cell growth. In support of this conclusion, a neutralizing antibody against the CCK peptide exhibited a dose dependent inhibition of cell growth whereas, antagonists to CCK caused a dose depend inhibition of exogenous stimulated glioma cell growth in vitro, via the CCK-B receptor which is PKC activated. Assessment of apoptosis and proteasome activity were undertaken and we report that treatment with CCK antagonists decreased proteasome and increased caspase-3 activity. These data indicate that CCK peptide and CCK-B are abundant in human gliomas and they act to stimulate cell growth in an autocrine manner, primarily via the high affinity CCK-B receptor, which was blocked by antagonists to CCK, perhaps via apoptosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0143-4179
pubmed:author
pubmed:issnType
Print
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
255-65
pubmed:meshHeading
pubmed-meshheading:18423848-Autocrine Communication, pubmed-meshheading:18423848-Brain Neoplasms, pubmed-meshheading:18423848-Caspase 3, pubmed-meshheading:18423848-Cell Line, Tumor, pubmed-meshheading:18423848-Cell Proliferation, pubmed-meshheading:18423848-Cholecystokinin, pubmed-meshheading:18423848-Cyclic AMP, pubmed-meshheading:18423848-Dose-Response Relationship, Drug, pubmed-meshheading:18423848-Glioma, pubmed-meshheading:18423848-Humans, pubmed-meshheading:18423848-Hydrolysis, pubmed-meshheading:18423848-Paracrine Communication, pubmed-meshheading:18423848-Phosphatidylinositols, pubmed-meshheading:18423848-Proteasome Endopeptidase Complex, pubmed-meshheading:18423848-RNA, Messenger, pubmed-meshheading:18423848-Receptors, Cholecystokinin, pubmed-meshheading:18423848-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18423848-Thymidine
pubmed:year
2008
pubmed:articleTitle
Cholecystokinin (CCK) and CCK receptor expression by human gliomas: Evidence for an autocrine/paracrine stimulatory loop.
pubmed:affiliation
School of Health and Life Sciences, The Biomedical Chemistry Research Group, Aston University, Birmingham, UK. oikonomou_e@hotmail.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't