Linked Life Data

18854640

Source:http://linkedlifedata.com/resource/pubmed/id/18854640

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-3-11
pubmed:abstractText
Although endocrine disrupting chemicals (EDCs) may interfere with the endocrine system(s) of our body and have estrogenicity or androgenicity, the exact mechanism(s) underlying their detrimental effects is not clearly understood. Thus, in this study, we evaluated the effects of EDCs on proliferation and regulation of transcription of estrogen receptor (ER)-positive BG-1 ovarian cancer cells, and their possible mechanisms were further examined. Treatment with bisphenol A (BPA), nonylphenol (NP), octylphenol (OP) and methoxychlor (MXC) for 24 h resulted in an increase of cell proliferation. Treatment with BPA, NP, OP and MXC increased the estrogen response element (ERE) activity. The increase of cell proliferation and activation of ERE were reversed in the presence of an estrogen receptor antagonist, ICI 182780. These results suggest that ER is involved in EDC-mediated pathway in ovarian cancer cells. Based on this, we further investigated the involvement of EDCs in activation of mitogen-activated protein kinase (MAPK) in relation to cell growth. BPA rapidly induced activation of extracellular signal-regulated kinase (ERK) 1/2 and p38 MAPK at 15 min, but the effect of BPA (10 microM) on stimulation of cell growth was not blocked by pretreatment with inhibitors of MEK (PD98059) or p38 (SB203580) in a dose-dependent manner. Taken together, EDC-induced proliferation is mediated by a genomic effect through ERs and ERE, but EDC-activated MAPK is unlikely to be involved in EDC-induced cell growth in estrogen-responsive ovarian cancer cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0916-8818
pubmed:author
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
23-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18854640-Cell Growth Processes, pubmed-meshheading:18854640-Endocrine Disruptors, pubmed-meshheading:18854640-Enzyme Activation, pubmed-meshheading:18854640-Enzyme Inhibitors, pubmed-meshheading:18854640-Estrogens, pubmed-meshheading:18854640-Female, pubmed-meshheading:18854640-Flavonoids, pubmed-meshheading:18854640-Gene Expression Regulation, Neoplastic, pubmed-meshheading:18854640-Humans, pubmed-meshheading:18854640-Imidazoles, pubmed-meshheading:18854640-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:18854640-Ovarian Neoplasms, pubmed-meshheading:18854640-Pyridines, pubmed-meshheading:18854640-Receptors, Estrogen, pubmed-meshheading:18854640-Response Elements, pubmed-meshheading:18854640-Signal Transduction, pubmed-meshheading:18854640-Tumor Cells, Cultured, pubmed-meshheading:18854640-p38 Mitogen-Activated Protein Kinases
pubmed:year
2009
pubmed:articleTitle
Cell growth of ovarian cancer cells is stimulated by xenoestrogens through an estrogen-dependent pathway, but their stimulation of cell growth appears not to be involved in the activation of the mitogen-activated protein kinases ERK-1 and p38.
pubmed:affiliation
Department of Obstetrics and Gynecology, British Columbia Women's Hospital, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't