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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?
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.
Persistent Identifierhttp://hdl.handle.net/10722/168518
ISSN
2023 Impact Factor: 10.0
2023 SCImago Journal Rankings: 4.623
ISI Accession Number ID
References

 

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.pmid21350001-
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
dc.identifier.issnl1078-0432-

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