Linked Life Data

11559543

Source:http://linkedlifedata.com/resource/pubmed/id/11559543

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2001-9-17
pubmed:abstractText
Sphingolipid consumption suppresses colon carcinogenesis, but the specific genetic defect(s) that can be bypassed by these dietary components are not known. Colon tumors often have defect(s) in the adenomatous polyposis coli (APC)/beta-catenin regulatory system. Therefore, C57Bl/6J(Min/+) mice with a truncated APC gene product were fed diets supplemented with ceramide, sphingomyelin, glucosylceramide, lactosylceramide, and ganglioside G(D3) (a composition similar in amount and type to that of dairy products) to determine whether tumorigenesis caused by this category of genetic defect is suppressed. Sphingolipid feeding reduced the number of tumors in all regions of the intestine, and caused a marked redistribution of beta-catenin from a diffuse (cytosolic plus membrane) pattern to a more "normal" localization at mainly intercellular junctions between intestinal epithelial cells. The major digestion product of complex sphingolipids is sphingosine, and treatment of two human colon cancer cell lines in culture (SW480 and T84) with sphingosine reduced cytosolic and nuclear beta-catenin, inhibited growth, and induced cell death. Ceramides, particularly long-chain ceramides, also had effects. Thus, dietary sphingolipids, presumably via their digestion products, bypass or correct defect(s) in the APC/beta-catenin regulatory pathway. This may be at least one mechanism whereby dietary sphingolipids inhibit colon carcinogenesis, and might have implications for dietary intervention in human familial adenomatous polyposis and colon cancer.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6723-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11559543-Adenomatous Polyposis Coli Protein, pubmed-meshheading:11559543-Animals, pubmed-meshheading:11559543-Cattle, pubmed-meshheading:11559543-Cell Division, pubmed-meshheading:11559543-Cell Nucleus, pubmed-meshheading:11559543-Colonic Neoplasms, pubmed-meshheading:11559543-Cytoskeletal Proteins, pubmed-meshheading:11559543-Cytosol, pubmed-meshheading:11559543-Diet, pubmed-meshheading:11559543-Humans, pubmed-meshheading:11559543-Intestinal Neoplasms, pubmed-meshheading:11559543-Intestines, pubmed-meshheading:11559543-Male, pubmed-meshheading:11559543-Mice, pubmed-meshheading:11559543-Mice, Inbred C57BL, pubmed-meshheading:11559543-Signal Transduction, pubmed-meshheading:11559543-Sphingolipids, pubmed-meshheading:11559543-Sphingosine, pubmed-meshheading:11559543-Trans-Activators, pubmed-meshheading:11559543-Tumor Cells, Cultured, pubmed-meshheading:11559543-beta Catenin
pubmed:year
2001
pubmed:articleTitle
Modulation of intracellular beta-catenin localization and intestinal tumorigenesis in vivo and in vitro by sphingolipids.
pubmed:affiliation
Department of Biochemistry, Emory University School of Medicine, Atlanta, Georgia 30322-3050, USA. schmelze@karmanos.org
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't