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Conference Paper: Microrna-143 is a potential tumor suppressor targeting DNA methyltransferases 3A in breast cancer

TitleMicrorna-143 is a potential tumor suppressor targeting DNA methyltransferases 3A in breast cancer
Authors
KeywordsMedical sciences
Oncology
Issue Date2009
PublisherOxford University Press. The Journal's web site is located at http://annonc.oxfordjournals.org/
Citation
The IMPAKT Breast Cancer Conference, Brussels, Belgium, 7-9 May 2009. In Annals of Oncology, 2009, v. 20, suppl. 2, p. 41, abstract no. 111P How to Cite?
AbstractBACKGROUND AND AIMS: MicroRNAs (miRNAs) are 19-25-nucleotides regulatory non-protein-coding RNA molecules that regulate the expressions of a wide variety of genes including some involved in cancer development. Down-regulation of miR-143 has been reported in various human cancers including colorectal cancer and B-cell lymphomas. The aim of this study was to elucidate the role of miR-143 deregulation in breast cancer. METHODS: Down-regulation of miR-143 was evaluated in breast cancer cell lines and paired breast tumors and normal tissues by quantitative RT-PCR. Potential targets of miR-143 were defined. The functional effect of the miR-143 and its targets was performed in human breast cancer cell lines to confirm target association. RESULTS: Down-regulation of miR-143 was verified in both human breast cancer cell lines and 80% (12/15) of breast tumors (P < 0.001). Using in-silico predictions, DNA methyltranferase 3A (DNMT3A), one of a key enzyme involved in DNA methylation, was defined as a downstream potential target of miR-143. Restoration of miR-143 expression in breast cancer cell lines down-regulated expression of DNMT3A. DNMT3A was demonstrated to be a direct target of miR-143 by luciferase reporter assay. Expressions of DNMT3A and miR-143 were inversely correlated in tumor and normal breast tissues. CONCLUSIONS: In this study, we show for the first time that miR-143 specifically targeted DNMT3A and the expression of miR-143 was inversely correlated with DNMT3A expression in breast cancer. Our findings demonstrated that down-regulation of miR-143 and up-regulation of DNMT3A are significant changes in breast tumors. These findings point to a tumor suppressive role of miR-143 in epigenetic aberration of breast cancer, pointing to miRNA-based targeted approaches for breast cancer therapy.
DescriptionPoster area
Persistent Identifierhttp://hdl.handle.net/10722/126927
ISSN
2015 Impact Factor: 9.269
2015 SCImago Journal Rankings: 4.362

 

DC FieldValueLanguage
dc.contributor.authorKwong, Aen_HK
dc.contributor.authorNg, Een_HK
dc.contributor.authorTang, Een_HK
dc.contributor.authorWong, Cen_HK
dc.contributor.authorKwok, TTen_HK
dc.contributor.authorMa, Een_HK
dc.date.accessioned2010-10-31T12:56:37Z-
dc.date.available2010-10-31T12:56:37Z-
dc.date.issued2009en_HK
dc.identifier.citationThe IMPAKT Breast Cancer Conference, Brussels, Belgium, 7-9 May 2009. In Annals of Oncology, 2009, v. 20, suppl. 2, p. 41, abstract no. 111Pen_HK
dc.identifier.issn0923-7534en_HK
dc.identifier.urihttp://hdl.handle.net/10722/126927-
dc.descriptionPoster area-
dc.description.abstractBACKGROUND AND AIMS: MicroRNAs (miRNAs) are 19-25-nucleotides regulatory non-protein-coding RNA molecules that regulate the expressions of a wide variety of genes including some involved in cancer development. Down-regulation of miR-143 has been reported in various human cancers including colorectal cancer and B-cell lymphomas. The aim of this study was to elucidate the role of miR-143 deregulation in breast cancer. METHODS: Down-regulation of miR-143 was evaluated in breast cancer cell lines and paired breast tumors and normal tissues by quantitative RT-PCR. Potential targets of miR-143 were defined. The functional effect of the miR-143 and its targets was performed in human breast cancer cell lines to confirm target association. RESULTS: Down-regulation of miR-143 was verified in both human breast cancer cell lines and 80% (12/15) of breast tumors (P < 0.001). Using in-silico predictions, DNA methyltranferase 3A (DNMT3A), one of a key enzyme involved in DNA methylation, was defined as a downstream potential target of miR-143. Restoration of miR-143 expression in breast cancer cell lines down-regulated expression of DNMT3A. DNMT3A was demonstrated to be a direct target of miR-143 by luciferase reporter assay. Expressions of DNMT3A and miR-143 were inversely correlated in tumor and normal breast tissues. CONCLUSIONS: In this study, we show for the first time that miR-143 specifically targeted DNMT3A and the expression of miR-143 was inversely correlated with DNMT3A expression in breast cancer. Our findings demonstrated that down-regulation of miR-143 and up-regulation of DNMT3A are significant changes in breast tumors. These findings point to a tumor suppressive role of miR-143 in epigenetic aberration of breast cancer, pointing to miRNA-based targeted approaches for breast cancer therapy.-
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://annonc.oxfordjournals.org/-
dc.relation.ispartofAnnals of Oncologyen_HK
dc.subjectMedical sciences-
dc.subjectOncology-
dc.titleMicrorna-143 is a potential tumor suppressor targeting DNA methyltransferases 3A in breast canceren_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0923-7534&volume=20, suppl. 2&spage=ii41, abstract no. 111P&epage=&date=2009&atitle=Microrna-143+is+a+potential+tumor+suppressor+targeting+DNA+methyltransferases+3A+in+breast+canceren_HK
dc.identifier.emailKwong, A: avakwong@HKUCC.hku.hken_HK
dc.identifier.emailNg, E: enders.ng@gmail.comen_HK
dc.identifier.emailTang, E: etanga@alumni.sfu.caen_HK
dc.identifier.emailKwok, TT: kwok2020@cuhk.edu.hken_HK
dc.identifier.emailMa, E: eskma@HKUCC.hku.hk-
dc.description.natureabstract-
dc.identifier.doi10.1093/annonc/mdp102-
dc.identifier.hkuros181440en_HK
dc.identifier.hkuros164482-
dc.identifier.hkuros164474-
dc.identifier.volume20en_HK
dc.identifier.issuesuppl. 2-
dc.identifier.spage41en_HK
dc.identifier.epage41en_HK
dc.description.otherThe IMPAKT Breast Cancer Conference, Brussels, Belgium, 7-9 May 2009. In Annals of Oncology, 2009, v. 20, suppl. 2, p. 41, abstract no. 111P-

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