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Conference Paper: An isogenic experimental model identifies β-catenin as a molecular target in ovarian cancer metastasis

TitleAn isogenic experimental model identifies β-catenin as a molecular target in ovarian cancer metastasis
Other TitlesAn isogenic experimental model identifies b-catenin as a molecular target in ovarian cancer metastasis
Authors
Issue Date2016
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 107th Annual Meeting of the American Association for Cancer Research (AACR 2016), New Orleans, LA., 16-20 April 2016. In Cancer Research, 2016, v. 76 n. 14 suppl., abstract no. 650 How to Cite?
AbstractOvarian cancer metastasis is closely associated with unfavorable outcomes, yet the underlying mechanisms remain obscure. Here we establish an isogenic model that could mimic the spontaneous metastasis of human ovarian cancer. Given that tumor cells are heterogeneous in nature, an isogenic pair of highly metastatic (HM) and non-metastatic (NM) cell lines with opposite metastatic capabilities was derived using in vitro and in vivo selection. Incorporation of the luciferase gene into the cell pair allowed non-invasive monitoring of the metastatic events by bioluminescent imaging in vivo. Orthotopic implantation of HM into the ovarian bursa of NOD/SCID mice resulted in metastases within the peritoneum with ascites formation, thus representing the major dissemination pattern of human ovarian cancer cells. However, NM failed to form detectable metastases, although it was tumorigenic at the ovarian bursa. In comparison with NM, HM displayed higher spheroid-forming ability and had higher expression of stemness marker genes, which are characteristics of cancer stem-like population. By proteomic profiling and pathway analysis, HM is found to be enriched in the oncogenic β-catenin signaling, a pathway elevated in ovarian cancer metastases. Tumor initiation and metastasis of HM was dramatically impaired when β-catenin was specifically knocked down. We further demonstrated that β-catenin could down-regulate the expression of Dicer, a major component of the microRNA machinery. These results together suggest that this model could help to delineate the molecular mechanisms for ovarian cancer metastasis, and provide clinically relevant insights to target metastasizing ovarian cancer cells. ©2016 American Association for Cancer Research.
DescriptionSession - Tumor Biology: no. 650
This journal suppl. entitled: Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA
Persistent Identifierhttp://hdl.handle.net/10722/229948
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorTo, SKY-
dc.contributor.authorWong, AST-
dc.date.accessioned2016-08-23T14:14:15Z-
dc.date.available2016-08-23T14:14:15Z-
dc.date.issued2016-
dc.identifier.citationThe 107th Annual Meeting of the American Association for Cancer Research (AACR 2016), New Orleans, LA., 16-20 April 2016. In Cancer Research, 2016, v. 76 n. 14 suppl., abstract no. 650-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/229948-
dc.descriptionSession - Tumor Biology: no. 650-
dc.descriptionThis journal suppl. entitled: Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA-
dc.description.abstractOvarian cancer metastasis is closely associated with unfavorable outcomes, yet the underlying mechanisms remain obscure. Here we establish an isogenic model that could mimic the spontaneous metastasis of human ovarian cancer. Given that tumor cells are heterogeneous in nature, an isogenic pair of highly metastatic (HM) and non-metastatic (NM) cell lines with opposite metastatic capabilities was derived using in vitro and in vivo selection. Incorporation of the luciferase gene into the cell pair allowed non-invasive monitoring of the metastatic events by bioluminescent imaging in vivo. Orthotopic implantation of HM into the ovarian bursa of NOD/SCID mice resulted in metastases within the peritoneum with ascites formation, thus representing the major dissemination pattern of human ovarian cancer cells. However, NM failed to form detectable metastases, although it was tumorigenic at the ovarian bursa. In comparison with NM, HM displayed higher spheroid-forming ability and had higher expression of stemness marker genes, which are characteristics of cancer stem-like population. By proteomic profiling and pathway analysis, HM is found to be enriched in the oncogenic β-catenin signaling, a pathway elevated in ovarian cancer metastases. Tumor initiation and metastasis of HM was dramatically impaired when β-catenin was specifically knocked down. We further demonstrated that β-catenin could down-regulate the expression of Dicer, a major component of the microRNA machinery. These results together suggest that this model could help to delineate the molecular mechanisms for ovarian cancer metastasis, and provide clinically relevant insights to target metastasizing ovarian cancer cells. ©2016 American Association for Cancer Research.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.titleAn isogenic experimental model identifies β-catenin as a molecular target in ovarian cancer metastasis-
dc.title.alternativeAn isogenic experimental model identifies b-catenin as a molecular target in ovarian cancer metastasis-
dc.typeConference_Paper-
dc.identifier.emailTo, SKY: tokityan@hku.hk-
dc.identifier.emailMak, ASC: ascmak@hkucc.hku.hk-
dc.identifier.emailFung, EYM: eva.fungym@hku.hk-
dc.identifier.emailChe, CM: chemhead@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.emailWong, AST: awong1@hku.hk-
dc.identifier.authorityFung, EYM=rp01986-
dc.identifier.authorityChe, CM=rp00670-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.authorityWong, AST=rp00805-
dc.identifier.doi10.1158/1538-7445.AM2016-650-
dc.identifier.hkuros260463-
dc.identifier.volume76-
dc.identifier.issue14 suppl.-
dc.publisher.placeUnited States-

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