Linked Life Data

14611671

Source:http://linkedlifedata.com/resource/pubmed/id/14611671

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2003-11-12
pubmed:abstractText
Epithelial ovarian carcinomas are thought to arise from cells of ovarian surface epithelium (OSE) covering the free surface of the human ovary. Two immortalized human cell lines, OSE2a (non-tumorigenic) and OSE2b-2 (tumorigenic), were previously established from normal OSE cells of a reproductive-age patient. In the present study, we found that expression of luteinizing hormone (LH)/chorionic gonadotropin (CG) receptor (LH/CGR) is present in OSE2a cells and absent in OSE2b-2 cells. In OSE2a cells, a low concentration (10(3) mIU/ml) of CG enhanced anchorage-dependent growth via up-regulation of insulin-like growth factor-1 (IGF1), whereas a high concentration (10(5) mIU/ml) of CG induced anchorage-independent growth and down-regulation of IGF1 expression. To investigate involvement of other genes in LH/CGR-related tumorigenicity, we compared cDNA expression arrays of OSE2a and OSE2b-2 cells, and found that the following genes had lower expression in OSE2b-2 than in OSE2a: integrin beta 1, intercellular adhesion molecule-1 (ICAM1), and Waf1/Cip1. Subsequent semiquantitative reverse transcription polymerase chain reaction using OSE2a cells showed that expression of integrin beta 1 was down-regulated by a high concentration (10(5) mIU/ml) of CG. These results suggest that LH/CGR affects anchorage-dependent and -independent growth by mediating up- and down-regulation of IGF1 and integrin beta 1. Repetitive and excessive activation of LH/CGR may cause genetic alteration of its signal transduction pathway, resulting in stimulation of growth of OSE cells, initiation of ovarian carcinogenesis, and cancer progression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1347-9032
pubmed:author
pubmed:issnType
Print
pubmed:volume
94
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
953-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:14611671-Antigens, CD29, pubmed-meshheading:14611671-Cell Adhesion, pubmed-meshheading:14611671-Cell Division, pubmed-meshheading:14611671-Cells, Cultured, pubmed-meshheading:14611671-Chorionic Gonadotropin, pubmed-meshheading:14611671-Colony-Forming Units Assay, pubmed-meshheading:14611671-Cyclin-Dependent Kinase Inhibitor p21, pubmed-meshheading:14611671-Cyclins, pubmed-meshheading:14611671-Epithelial Cells, pubmed-meshheading:14611671-Female, pubmed-meshheading:14611671-Humans, pubmed-meshheading:14611671-Insulin-Like Growth Factor I, pubmed-meshheading:14611671-Intercellular Adhesion Molecule-1, pubmed-meshheading:14611671-Luteinizing Hormone, pubmed-meshheading:14611671-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:14611671-Ovary, pubmed-meshheading:14611671-Receptors, LH, pubmed-meshheading:14611671-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:14611671-Signal Transduction
pubmed:year
2003
pubmed:articleTitle
Roles of luteinizing hormone/chorionic gonadotropin receptor in anchorage-dependent and -independent growth in human ovarian surface epithelial cell lines.
pubmed:affiliation
Department of Obstetrics and Gynecology, Kumamoto University School of Medicine, Kumumoto City, Kumamoto 860-8556.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't