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Conference Paper: MiRNA-199A-5P is a biomarker for and regulator of epithelial-mesenchymal transition in triple negative breast cancer patients

TitleMiRNA-199A-5P is a biomarker for and regulator of epithelial-mesenchymal transition in triple negative breast cancer patients
Authors
KeywordsMedical sciences
Communicable diseases
Issue Date2014
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://www.aacrmeetingabstracts.org/
Citation
The 105th Annual Meeting of the American Association for Cancer Research (AACR 2014), San Diego, CA., 5-9 April 2014. In AACR Meeting Abstracts, 2014, v. 74 n. 19 suppl., abstract no. 531 How to Cite?
AbstractObjectives: Triple-negative breast cancer (TNBC) accounts for 15-20% of all breast cancer, and is characterized by the absence of estrogen receptor, progesterone receptor and human epidermal growth factor receptor. The lack of targeted therapy is a major obstacle for treating against this aggressive subtype, hence the search of specific biomarkers may use as potential diagnostic marker and perhaps a therapeutic target for TNBC. Methods: Plasma samples from patients with TNBC and non-TNBC were recruited for miRNA profiling. By using miRCURY LNA array containing 730 miRNAs, we compared the differential miRNA expressions in plasma of patient with TNBC (n=5) and non-TNBC (n=5), as well as healthy controls (n=5). Selected miRNAs were further validated in an independent cohort (n=250) using real-time RT-PCR. Functional study of miRNA was also carried out in the cell lines. Results: Microarray data revealed miR-16, miR-21 and miR-199a-5p have differentially expression between TNBC and non-TNBC. We found that miR-16, miR-21 and miR-199a-5p were underexpressed in TNBC cases when compared with healthy controls. Moreover, post-operative expression levels of miR-16, miR-21 and miR-199a-5p were significantly increased than that of pre-operative plasma of TNBC. We then stratified the patients by TNM stage and associate with miRNA expression level. Plasma miR-199a-5p expression in TNBC patients had significant difference when compared with healthy controls (stage I, p<0.002; stage II, p<0.001; stage III, p<0.011). Transfection of miR-199a-5p mimic significantly reduced cell proliferation and restored the epithelial-mesenchymal transition (EMT) markers (E-cadherin, ZEB1 and TWIST2). Conclusions: Our data implicate that miR-199a-5p is a potential marker for discriminating TNBC cases and non-TNBC cases. The association of miR-199a-5p with EMT markers uncovers an important pathway in metastatic breast cancer. This study provides insights for the potential use of miRNA as diagnostic marker and targeted therapy for the treatment of TNBC.
DescriptionPoster presentation: abstract no. 531
Persistent Identifierhttp://hdl.handle.net/10722/217642
ISSN

 

DC FieldValueLanguage
dc.contributor.authorShin, VY-
dc.contributor.authorSiu, JMT-
dc.contributor.authorHo, CWJ-
dc.contributor.authorKwong, A-
dc.date.accessioned2015-09-18T06:08:20Z-
dc.date.available2015-09-18T06:08:20Z-
dc.date.issued2014-
dc.identifier.citationThe 105th Annual Meeting of the American Association for Cancer Research (AACR 2014), San Diego, CA., 5-9 April 2014. In AACR Meeting Abstracts, 2014, v. 74 n. 19 suppl., abstract no. 531-
dc.identifier.issn1948-3279-
dc.identifier.urihttp://hdl.handle.net/10722/217642-
dc.descriptionPoster presentation: abstract no. 531-
dc.description.abstractObjectives: Triple-negative breast cancer (TNBC) accounts for 15-20% of all breast cancer, and is characterized by the absence of estrogen receptor, progesterone receptor and human epidermal growth factor receptor. The lack of targeted therapy is a major obstacle for treating against this aggressive subtype, hence the search of specific biomarkers may use as potential diagnostic marker and perhaps a therapeutic target for TNBC. Methods: Plasma samples from patients with TNBC and non-TNBC were recruited for miRNA profiling. By using miRCURY LNA array containing 730 miRNAs, we compared the differential miRNA expressions in plasma of patient with TNBC (n=5) and non-TNBC (n=5), as well as healthy controls (n=5). Selected miRNAs were further validated in an independent cohort (n=250) using real-time RT-PCR. Functional study of miRNA was also carried out in the cell lines. Results: Microarray data revealed miR-16, miR-21 and miR-199a-5p have differentially expression between TNBC and non-TNBC. We found that miR-16, miR-21 and miR-199a-5p were underexpressed in TNBC cases when compared with healthy controls. Moreover, post-operative expression levels of miR-16, miR-21 and miR-199a-5p were significantly increased than that of pre-operative plasma of TNBC. We then stratified the patients by TNM stage and associate with miRNA expression level. Plasma miR-199a-5p expression in TNBC patients had significant difference when compared with healthy controls (stage I, p<0.002; stage II, p<0.001; stage III, p<0.011). Transfection of miR-199a-5p mimic significantly reduced cell proliferation and restored the epithelial-mesenchymal transition (EMT) markers (E-cadherin, ZEB1 and TWIST2). Conclusions: Our data implicate that miR-199a-5p is a potential marker for discriminating TNBC cases and non-TNBC cases. The association of miR-199a-5p with EMT markers uncovers an important pathway in metastatic breast cancer. This study provides insights for the potential use of miRNA as diagnostic marker and targeted therapy for the treatment of TNBC.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://www.aacrmeetingabstracts.org/-
dc.relation.ispartofAACR Meeting Abstracts-
dc.subjectMedical sciences-
dc.subjectCommunicable diseases-
dc.titleMiRNA-199A-5P is a biomarker for and regulator of epithelial-mesenchymal transition in triple negative breast cancer patients-
dc.typeConference_Paper-
dc.identifier.emailShin, VY: vyshin@hku.hk-
dc.identifier.emailSiu, JMT: jensiu@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.AM2014-531-
dc.identifier.hkuros252017-
dc.identifier.volume74-
dc.identifier.issue19 suppl.-
dc.publisher.placeUnited States-

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