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Article: Aberrant activation of hedgehog signaling pathway in ovarian cancers: Effect on prognosis, cell invasion and differentiation
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TitleAberrant activation of hedgehog signaling pathway in ovarian cancers: Effect on prognosis, cell invasion and differentiation
 
AuthorsLiao, X1
Siu, MKY1
Au, CWH1
Wong, ESY1
Chan, HY1
Ip, PPC1
Ngan, HYS1
Cheung, ANY1
 
Issue Date2009
 
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
CitationCarcinogenesis, 2009, v. 30 n. 1, p. 131-140 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgn230
 
AbstractAberrant activation of hedgehog (HH) pathway has been implicated in the development of human malignancies. This study aimed at investigating the role of HH molecules in human ovarian carcinogenesis. The expression profiles of HH molecules were examined in ovarian tumor samples and ovarian cancer cell lines and the in vitro effects of HH molecules on cell proliferation, apoptosis, migration, invasion and cell differentiation as well as related downstream target genes were assessed. Overexpression of Patched and Gli1 protein in ovarian cancers correlated with poor survival of the patients (P = 0.008; P = 0.004). Significantly elevated expression of Sonic hedgehog messenger RNA was observed in ovarian cancers compared with normal tissues and benign ovarian tumors and such differential expression was specific to histological types (P < 0.05). Ectopic Gli1 overexpression in ovarian cancer cells conferred increased cell proliferation, cell mobility, invasiveness and change in differentiation in association with increased expression of E-cadherin, vimentin, Bcl-2, caspases as well as β1 integrin, membrane type 1 matrix metalloproteinase (MT1-MMP) and vascular endothelial growth factor (VEGF). Treatment with 3-keto-N-(aminoethyl-aminocaproyl-dihydrocinnamoyl)-cyclopamine induced cancer cell apoptosis, suppressed cell growth, mobility and invasiveness and induced cancer cell dedifferentiation with decreased expression of E-cadherin, cytokeratin 7, Snail, calretinin, vimentin, Bcl-2, caspases, β1 integrin, MT1-MMP and VEGF. Our data suggested that abnormal HH signaling activation plays important roles in the development and progression of ovarian cancers. Gli1 expression is an independent prognostic marker. Inhibition of the HH pathway molecules might be a valid therapeutic strategy for ovarian cancers. © The Author 2008. Published by Oxford University Press. All rights reserved.
 
ISSN0143-3334
2012 Impact Factor: 5.635
2012 SCImago Journal Rankings: 2.349
 
DOIhttp://dx.doi.org/10.1093/carcin/bgn230
 
ISI Accession Number IDWOS:000262718300018
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLiao, X
 
dc.contributor.authorSiu, MKY
 
dc.contributor.authorAu, CWH
 
dc.contributor.authorWong, ESY
 
dc.contributor.authorChan, HY
 
dc.contributor.authorIp, PPC
 
dc.contributor.authorNgan, HYS
 
dc.contributor.authorCheung, ANY
 
dc.date.accessioned2010-05-31T04:09:15Z
 
dc.date.available2010-05-31T04:09:15Z
 
dc.date.issued2009
 
dc.description.abstractAberrant activation of hedgehog (HH) pathway has been implicated in the development of human malignancies. This study aimed at investigating the role of HH molecules in human ovarian carcinogenesis. The expression profiles of HH molecules were examined in ovarian tumor samples and ovarian cancer cell lines and the in vitro effects of HH molecules on cell proliferation, apoptosis, migration, invasion and cell differentiation as well as related downstream target genes were assessed. Overexpression of Patched and Gli1 protein in ovarian cancers correlated with poor survival of the patients (P = 0.008; P = 0.004). Significantly elevated expression of Sonic hedgehog messenger RNA was observed in ovarian cancers compared with normal tissues and benign ovarian tumors and such differential expression was specific to histological types (P < 0.05). Ectopic Gli1 overexpression in ovarian cancer cells conferred increased cell proliferation, cell mobility, invasiveness and change in differentiation in association with increased expression of E-cadherin, vimentin, Bcl-2, caspases as well as β1 integrin, membrane type 1 matrix metalloproteinase (MT1-MMP) and vascular endothelial growth factor (VEGF). Treatment with 3-keto-N-(aminoethyl-aminocaproyl-dihydrocinnamoyl)-cyclopamine induced cancer cell apoptosis, suppressed cell growth, mobility and invasiveness and induced cancer cell dedifferentiation with decreased expression of E-cadherin, cytokeratin 7, Snail, calretinin, vimentin, Bcl-2, caspases, β1 integrin, MT1-MMP and VEGF. Our data suggested that abnormal HH signaling activation plays important roles in the development and progression of ovarian cancers. Gli1 expression is an independent prognostic marker. Inhibition of the HH pathway molecules might be a valid therapeutic strategy for ovarian cancers. © The Author 2008. Published by Oxford University Press. All rights reserved.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationCarcinogenesis, 2009, v. 30 n. 1, p. 131-140 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgn230
 
dc.identifier.doihttp://dx.doi.org/10.1093/carcin/bgn230
 
dc.identifier.epage140
 
dc.identifier.hkuros166975
 
dc.identifier.isiWOS:000262718300018
 
dc.identifier.issn0143-3334
2012 Impact Factor: 5.635
2012 SCImago Journal Rankings: 2.349
 
dc.identifier.issue1
 
dc.identifier.openurl
 
dc.identifier.pmid19028702
 
dc.identifier.scopuseid_2-s2.0-58949100355
 
dc.identifier.spage131
 
dc.identifier.urihttp://hdl.handle.net/10722/60368
 
dc.identifier.volume30
 
dc.languageeng
 
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofCarcinogenesis
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCarcinogenesis. Copyright © Lippincott Williams & Wilkins.
 
dc.subject.meshCell Differentiation
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshFemale
 
dc.subject.meshHedgehog Proteins - metabolism
 
dc.subject.meshHumans
 
dc.subject.meshImmunohistochemistry
 
dc.subject.meshNeoplasm Invasiveness
 
dc.subject.meshOvarian Neoplasms - metabolism - pathology
 
dc.subject.meshPrognosis
 
dc.subject.meshReceptors, Cell Surface - metabolism
 
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction
 
dc.subject.meshSignal Transduction
 
dc.subject.meshTranscription Factors - metabolism
 
dc.titleAberrant activation of hedgehog signaling pathway in ovarian cancers: Effect on prognosis, cell invasion and differentiation
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong