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Article: Analysis of MiR-195 and MiR-497 expression, regulation and role in breast cancer

TitleAnalysis of MiR-195 and MiR-497 expression, regulation and role in breast cancer
Authors
Issue Date2011
Citation
Clinical Cancer Research, 2011, v. 17 n. 7, p. 1722-1730 How to Cite?
Abstract
Purpose: To investigate expression, regulation, potential role and targets of miR-195 and miR-497 in breast cancer. Experimental Design: The expression patterns of miR-195 and miR-497 were initially examined in breast cancer tissues and cell lines by Northern blotting and quantitative real-time PCR. Combined bisulfite restriction analysis and bisulfite sequencing were carried out to study the DNA methylation status of miR-195 and miR-497 genes. Breast cancer cells stably expressing miR-195 and miR-497 were established to study their role and targets. Finally, normal, fibroadenoma and breast cancer tissues were employed to analyze the correlation between miR-195/497 levels and malignant stages of breast tumor tissues. Results: MiR-195 and miR-497 were significantly downregulated in breast cancer. The methylation state of CpG islands upstream of the miR-195/497 gene was found to be responsible for the downregulation of both miRNAs. Forced expression of miR-195 or miR-497 suppressed breast cancer cell proliferation and invasion. Raf-1 and Ccnd1 were identified as novel direct targets of miR-195 and miR-497. miR-195/497 expression levels in clinical specimens were found to be correlated inversely with malignancy of breast cancer. Conclusions: Our data imply that both miR-195 and miR-497 play important inhibitory roles in breast cancer malignancy and may be the potential therapeutic and diagnostic targets. ©2011 AACR.
Persistent Identifierhttp://hdl.handle.net/10722/168518
ISSN
2013 Impact Factor: 8.193
2013 SCImago Journal Rankings: 5.150
ISI Accession Number ID
References

 

Author Affiliations
  1. Peking Union Medical College
  2. Nanjing Medical University
  3. Chinese Academy of Sciences
  4. Fudan University Shanghai Medical College
  5. Thomas Jefferson University
  6. East China Normal University
  7. Chinese University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorLi, Den_US
dc.contributor.authorZhao, Yen_US
dc.contributor.authorLiu, Cen_US
dc.contributor.authorChen, Xen_US
dc.contributor.authorQi, Yen_US
dc.contributor.authorJiang, Yen_US
dc.contributor.authorZou, Cen_US
dc.contributor.authorZhang, Xen_US
dc.contributor.authorLiu, Sen_US
dc.contributor.authorWang, Xen_US
dc.contributor.authorZhao, Den_US
dc.contributor.authorSun, Qen_US
dc.contributor.authorZeng, Zen_US
dc.contributor.authorDress, Aen_US
dc.contributor.authorLin, MCen_US
dc.contributor.authorKung, HFen_US
dc.contributor.authorRui, Hen_US
dc.contributor.authorLiu, LZen_US
dc.contributor.authorMao, Fen_US
dc.contributor.authorJiang, BHen_US
dc.contributor.authorLai, Len_US
dc.date.accessioned2012-10-08T03:19:56Z-
dc.date.available2012-10-08T03:19:56Z-
dc.date.issued2011en_US
dc.identifier.citationClinical Cancer Research, 2011, v. 17 n. 7, p. 1722-1730en_US
dc.identifier.issn1078-0432en_US
dc.identifier.urihttp://hdl.handle.net/10722/168518-
dc.description.abstractPurpose: To investigate expression, regulation, potential role and targets of miR-195 and miR-497 in breast cancer. Experimental Design: The expression patterns of miR-195 and miR-497 were initially examined in breast cancer tissues and cell lines by Northern blotting and quantitative real-time PCR. Combined bisulfite restriction analysis and bisulfite sequencing were carried out to study the DNA methylation status of miR-195 and miR-497 genes. Breast cancer cells stably expressing miR-195 and miR-497 were established to study their role and targets. Finally, normal, fibroadenoma and breast cancer tissues were employed to analyze the correlation between miR-195/497 levels and malignant stages of breast tumor tissues. Results: MiR-195 and miR-497 were significantly downregulated in breast cancer. The methylation state of CpG islands upstream of the miR-195/497 gene was found to be responsible for the downregulation of both miRNAs. Forced expression of miR-195 or miR-497 suppressed breast cancer cell proliferation and invasion. Raf-1 and Ccnd1 were identified as novel direct targets of miR-195 and miR-497. miR-195/497 expression levels in clinical specimens were found to be correlated inversely with malignancy of breast cancer. Conclusions: Our data imply that both miR-195 and miR-497 play important inhibitory roles in breast cancer malignancy and may be the potential therapeutic and diagnostic targets. ©2011 AACR.en_US
dc.languageengen_US
dc.relation.ispartofClinical Cancer Researchen_US
dc.subject.mesh3' Untranslated Regionsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshBreast Neoplasms - Genetics - Metabolism - Pathologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Movementen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshCpg Islandsen_US
dc.subject.meshCyclin D1 - Metabolismen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Silencingen_US
dc.subject.meshGenes, Reporteren_US
dc.subject.meshHumansen_US
dc.subject.meshLuciferases, Renilla - Biosynthesis - Geneticsen_US
dc.subject.meshMicrornas - Genetics - Metabolismen_US
dc.subject.meshNeoplasm Invasivenessen_US
dc.subject.meshProto-Oncogene Proteins C-Raf - Metabolismen_US
dc.subject.meshRestriction Mappingen_US
dc.titleAnalysis of MiR-195 and MiR-497 expression, regulation and role in breast canceren_US
dc.typeArticleen_US
dc.identifier.emailLin, MC:mcllin@hkucc.hku.hken_US
dc.identifier.authorityLin, MC=rp00746en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1158/1078-0432.CCR-10-1800en_US
dc.identifier.pmid21350001en_US
dc.identifier.scopuseid_2-s2.0-79953330808en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79953330808&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume17en_US
dc.identifier.issue7en_US
dc.identifier.spage1722en_US
dc.identifier.epage1730en_US
dc.identifier.isiWOS:000289054100010-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLi, D=46761212500en_US
dc.identifier.scopusauthoridZhao, Y=24170406900en_US
dc.identifier.scopusauthoridLiu, C=46761188300en_US
dc.identifier.scopusauthoridChen, X=24170717900en_US
dc.identifier.scopusauthoridQi, Y=24171887800en_US
dc.identifier.scopusauthoridJiang, Y=36673053600en_US
dc.identifier.scopusauthoridZou, C=36505538900en_US
dc.identifier.scopusauthoridZhang, X=46761651600en_US
dc.identifier.scopusauthoridLiu, S=46761178500en_US
dc.identifier.scopusauthoridWang, X=46761537900en_US
dc.identifier.scopusauthoridZhao, D=35147395100en_US
dc.identifier.scopusauthoridSun, Q=35206599000en_US
dc.identifier.scopusauthoridZeng, Z=7402647166en_US
dc.identifier.scopusauthoridDress, A=23145163000en_US
dc.identifier.scopusauthoridLin, MC=7404816359en_US
dc.identifier.scopusauthoridKung, HF=7402514190en_US
dc.identifier.scopusauthoridRui, H=7005244652en_US
dc.identifier.scopusauthoridLiu, LZ=35074383300en_US
dc.identifier.scopusauthoridMao, F=36461384700en_US
dc.identifier.scopusauthoridJiang, BH=35264238500en_US
dc.identifier.scopusauthoridLai, L=12445800200en_US

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