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Article: Pigment epithelium-derived factor is estrogen sensitive and inhibits the growth of human ovarian cancer and ovarian surface epithelial cells

TitlePigment epithelium-derived factor is estrogen sensitive and inhibits the growth of human ovarian cancer and ovarian surface epithelial cells
Authors
Issue Date2006
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2006, v. 147 n. 9, p. 4179-4191 How to Cite?
AbstractEpithelial ovarian carcinoma is the most lethal gynecological cancer. However, little is known about the molecular mechanisms underlying the disease development and progression. In this study, we found that the expression of pigment epithelium-derived factor (PEDF) was greatly reduced in ovarian tumors and in ovarian cancer cell lines when compared with their normal precursor, ovarian surface epithelium (OSE). In addition, we showed that exogenous PEDF inhibited the growth of cultured human OSE as well as ovarian cancer cell lines, whereas targeted inhibition of endogenous PEDF using small interfering RNA or neutralizing PEDF antibody promoted the growth of these cells, confirming that the growth-inhibitory effect was PEDF specific. We also report for the first time that estrogen is an important upstream regulator of PEDF in human OSE. Treatment of the cultured cells with 17β-estradiol (E 2) inhibited the expression of PEDF protein and mRNA in a dose- and time-dependent manner, which could be reversed by the specific estrogen receptor antagonist, ICI 182,780, indicating that the regulation was estrogen receptor-mediated. We further showed that this down-regulation of PEDF gene transcription was a direct, primary effect of E 2. E 2 promoted OSE and ovarian cancer cell growth, whereas simultaneous treatment with E 2 and PEDF abrogated the estrogenic growth stimulation of these cells. This study is the first to demonstrate a role of PEDF in OSE biology and ovarian cancer and suggests that the loss of PEDF may e of relevance in carcinogenesis. Copyright © 2006 by The Endocrine Society.
Persistent Identifierhttp://hdl.handle.net/10722/87425
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, LWTen_HK
dc.contributor.authorAu, SCLen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorTombranTink, Jen_HK
dc.contributor.authorAuersperg, Nen_HK
dc.contributor.authorWong, ASTen_HK
dc.date.accessioned2010-09-06T09:29:30Z-
dc.date.available2010-09-06T09:29:30Z-
dc.date.issued2006en_HK
dc.identifier.citationEndocrinology, 2006, v. 147 n. 9, p. 4179-4191en_HK
dc.identifier.issn0013-7227en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87425-
dc.description.abstractEpithelial ovarian carcinoma is the most lethal gynecological cancer. However, little is known about the molecular mechanisms underlying the disease development and progression. In this study, we found that the expression of pigment epithelium-derived factor (PEDF) was greatly reduced in ovarian tumors and in ovarian cancer cell lines when compared with their normal precursor, ovarian surface epithelium (OSE). In addition, we showed that exogenous PEDF inhibited the growth of cultured human OSE as well as ovarian cancer cell lines, whereas targeted inhibition of endogenous PEDF using small interfering RNA or neutralizing PEDF antibody promoted the growth of these cells, confirming that the growth-inhibitory effect was PEDF specific. We also report for the first time that estrogen is an important upstream regulator of PEDF in human OSE. Treatment of the cultured cells with 17β-estradiol (E 2) inhibited the expression of PEDF protein and mRNA in a dose- and time-dependent manner, which could be reversed by the specific estrogen receptor antagonist, ICI 182,780, indicating that the regulation was estrogen receptor-mediated. We further showed that this down-regulation of PEDF gene transcription was a direct, primary effect of E 2. E 2 promoted OSE and ovarian cancer cell growth, whereas simultaneous treatment with E 2 and PEDF abrogated the estrogenic growth stimulation of these cells. This study is the first to demonstrate a role of PEDF in OSE biology and ovarian cancer and suggests that the loss of PEDF may e of relevance in carcinogenesis. Copyright © 2006 by The Endocrine Society.en_HK
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_HK
dc.relation.ispartofEndocrinologyen_HK
dc.rightsEndocrinology. Copyright © The Endocrine Society.en_HK
dc.subject.meshAntibodies - pharmacologyen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshCell Line, Transformeden_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshEpithelial Cells - pathologyen_HK
dc.subject.meshEstradiol - pharmacologyen_HK
dc.subject.meshEye Proteins - antagonists & inhibitors - genetics - pharmacologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression - drug effectsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshIn Situ Nick-End Labelingen_HK
dc.subject.meshNerve Growth Factors - antagonists & inhibitors - genetics - pharmacologyen_HK
dc.subject.meshOvarian Neoplasms - pathologyen_HK
dc.subject.meshOvary - pathologyen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshRNA, Messenger - analysisen_HK
dc.subject.meshRNA, Small Interfering - pharmacologyen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSerpins - genetics - pharmacologyen_HK
dc.titlePigment epithelium-derived factor is estrogen sensitive and inhibits the growth of human ovarian cancer and ovarian surface epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0013-7227&volume=147&spage=4179&epage=4191&date=2006&atitle=Pigment+epithelium-derived+factor+is+estrogen+sensitive+and+inhibits+the+growth+of+human+ovarian+cancer+and+ovarian+surface+epithelial+cellsen_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailWong, AST: awong1@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityWong, AST=rp00805en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/en.2006-0168en_HK
dc.identifier.pmid16777976-
dc.identifier.scopuseid_2-s2.0-33747602349en_HK
dc.identifier.hkuros120433en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33747602349&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume147en_HK
dc.identifier.issue9en_HK
dc.identifier.spage4179en_HK
dc.identifier.epage4191en_HK
dc.identifier.isiWOS:000239790100022-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, LWT=14119560800en_HK
dc.identifier.scopusauthoridAu, SCL=14119361300en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridTombranTink, J=7003724753en_HK
dc.identifier.scopusauthoridAuersperg, N=7006582556en_HK
dc.identifier.scopusauthoridWong, AST=23987963300en_HK

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