File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Prostaglandin E receptor 2 (EP2) regulates breast cancer stem-cell like property and promotes epithelial-mesenchymal transition

TitleProstaglandin E receptor 2 (EP2) regulates breast cancer stem-cell like property and promotes epithelial-mesenchymal transition
Authors
Issue Date2015
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 37th Annual CTRC-AACR San Antonio Breast Cancer Symposium, San Antonio, TX., 9-13 December 2014. In Cancer Research, 2015, v. 75 n. 9 suppl., abstract P2-07-07 How to Cite?
AbstractBACKGROUND: Presence of cancer stem-like cells (CSCs) is the main obstacle for poor treatment response and mortality in breast cancer patients. Prostaglandin E receptors have been reported to play a role in epithelial-mesenchymal transition (EMT) and metastasis, however, the contribution on cancer stem cell compartment remains unstudied. METHODS: Human xenograft breast cancer model was used to study the expression of EP receptors during cancer development. Construction of stable EP2-expression cells was used to study tumorigenesis and characterization of EP2 receptor. Functional role of EP2 receptor on cell proliferation, flow cyometry, invasion and EMT gene expression array were performed in transfected cells. Expression of EP2 receptor was compared in primary tumor tissues by immunostaining and real-time PCR. RESULTS: EP2 receptor was predominantly expressed in animal tissues during cancer development, as well as in human primary tumor tissues. In mouse xenograft model, MB-231-EP2 clone developed a more aggressive tumor with a larger tumor size and showed a significant increase in cancer stem cell marker aldehyde hydrogenase (ALDH1) expression. In vitro study, MB-231-EP2 clone increased colony formation capacity and S-phase entry by the regulation of E-cadherin, TWIST1 and ALDH1. Importantly, we found that Twist1 expression level was higher in breast cancer patients than healthy controls and was associated with ALDH1 expression. CONCLUSIONS: These findings implicated that EP2 receptor was crucial to nurture CSC phenotype and promote tumorigenesis in breast cancer. Blocking of EP2 might be a potential therapeutic strategy to improve treatment response for breast cancer patients.
DescriptionThis journal suppl. entitled: Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX
Poster Session 2: Tumor Cell and Molecular Biology: Epithelial-Mesenchymal Transition: no. P2-07-07
Persistent Identifierhttp://hdl.handle.net/10722/215347
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorShin, VY-
dc.contributor.authorSiu, JMT-
dc.contributor.authorHo, JCW-
dc.contributor.authorCheuk, IWY-
dc.contributor.authorChen, J-
dc.contributor.authorKwong, A-
dc.date.accessioned2015-08-21T13:22:50Z-
dc.date.available2015-08-21T13:22:50Z-
dc.date.issued2015-
dc.identifier.citationThe 37th Annual CTRC-AACR San Antonio Breast Cancer Symposium, San Antonio, TX., 9-13 December 2014. In Cancer Research, 2015, v. 75 n. 9 suppl., abstract P2-07-07-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/215347-
dc.descriptionThis journal suppl. entitled: Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX-
dc.descriptionPoster Session 2: Tumor Cell and Molecular Biology: Epithelial-Mesenchymal Transition: no. P2-07-07-
dc.description.abstractBACKGROUND: Presence of cancer stem-like cells (CSCs) is the main obstacle for poor treatment response and mortality in breast cancer patients. Prostaglandin E receptors have been reported to play a role in epithelial-mesenchymal transition (EMT) and metastasis, however, the contribution on cancer stem cell compartment remains unstudied. METHODS: Human xenograft breast cancer model was used to study the expression of EP receptors during cancer development. Construction of stable EP2-expression cells was used to study tumorigenesis and characterization of EP2 receptor. Functional role of EP2 receptor on cell proliferation, flow cyometry, invasion and EMT gene expression array were performed in transfected cells. Expression of EP2 receptor was compared in primary tumor tissues by immunostaining and real-time PCR. RESULTS: EP2 receptor was predominantly expressed in animal tissues during cancer development, as well as in human primary tumor tissues. In mouse xenograft model, MB-231-EP2 clone developed a more aggressive tumor with a larger tumor size and showed a significant increase in cancer stem cell marker aldehyde hydrogenase (ALDH1) expression. In vitro study, MB-231-EP2 clone increased colony formation capacity and S-phase entry by the regulation of E-cadherin, TWIST1 and ALDH1. Importantly, we found that Twist1 expression level was higher in breast cancer patients than healthy controls and was associated with ALDH1 expression. CONCLUSIONS: These findings implicated that EP2 receptor was crucial to nurture CSC phenotype and promote tumorigenesis in breast cancer. Blocking of EP2 might be a potential therapeutic strategy to improve treatment response for breast cancer patients.-
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.titleProstaglandin E receptor 2 (EP2) regulates breast cancer stem-cell like property and promotes epithelial-mesenchymal transition-
dc.typeConference_Paper-
dc.identifier.emailShin, VY: vyshin@hku.hk-
dc.identifier.emailSiu, JMT: jensiu@hku.hk-
dc.identifier.emailCheuk, IWY: isacheuk@hku.hk-
dc.identifier.emailChen, J: gary0526@hku.hk-
dc.identifier.emailKwong, A: avakwong@hkucc.hku.hk-
dc.identifier.authorityShin, VY=rp02000-
dc.identifier.authorityKwong, A=rp01734-
dc.identifier.doi10.1158/1538-7445.SABCS14-P2-07-07-
dc.identifier.hkuros249277-
dc.identifier.volume75-
dc.identifier.issue9 suppl.-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats