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Article: Epigenetic inactivation of the MIR34B/C in multiple myeloma

TitleEpigenetic inactivation of the MIR34B/C in multiple myeloma
Authors
Issue Date2011
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 2011, v. 118 n. 22, p. 5901-5904 How to Cite?
Abstract
We postulated that MIR34B/C, a direct transcriptional target of TP53, might be inactivated by promoter hypermethylation in multiple myeloma (MM). MIR34B/C promoter methylation was studied in 8 normal marrow controls, 8 MM cell lines, 95 diagnostic, and 23 relapsed/progressed MMsamples by methylation-specific PCR. MIR34B/C was methylated in 6 (75.0%) MM cell lines but not normal controls. 5-Aza-2′-deoxycytidine led to MIR34B/C promoter demethylation and MIR34B reexpression. Moreover, restoration of MIR34B led to reduced cellular proliferation and enhanced apoptosis of myeloma cells. In primary samples, methylation of MIR34B/C occurred in 5.3% at diagnosis and 52.2% at relapse/disease progression (P < .001). In 12 MM patients with paired samples at diagnosis and relapse/progression, MIR34B/C methylation was acquired in 6 at relapse/progression. In conclusion, MIR34B/C is a tumor suppressor in myeloma. Hypermethylation of MIR34B/C is tumor-specific. Frequent MIR34B/C hypermethylation during relapse/progression but not at diagnosis implicated a role of MIR34B/C hypermethylation in myeloma relapse/progression. © 2011 by The American Society of Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/148661
ISSN
2013 Impact Factor: 9.775
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants Council763409M
Funding Information:

This work was supported by the Hong Kong Research Grants Council General Research Fund (#763409M).

References

 

Author Affiliations
  1. The University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorWong, KYen_HK
dc.contributor.authorYim, RLHen_HK
dc.contributor.authorSo, CCen_HK
dc.contributor.authorJin, DYen_HK
dc.contributor.authorLiang, Ren_HK
dc.contributor.authorChim, CSen_HK
dc.date.accessioned2012-05-29T06:14:30Z-
dc.date.available2012-05-29T06:14:30Z-
dc.date.issued2011en_HK
dc.identifier.citationBlood, 2011, v. 118 n. 22, p. 5901-5904en_HK
dc.identifier.issn0006-4971en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148661-
dc.description.abstractWe postulated that MIR34B/C, a direct transcriptional target of TP53, might be inactivated by promoter hypermethylation in multiple myeloma (MM). MIR34B/C promoter methylation was studied in 8 normal marrow controls, 8 MM cell lines, 95 diagnostic, and 23 relapsed/progressed MMsamples by methylation-specific PCR. MIR34B/C was methylated in 6 (75.0%) MM cell lines but not normal controls. 5-Aza-2′-deoxycytidine led to MIR34B/C promoter demethylation and MIR34B reexpression. Moreover, restoration of MIR34B led to reduced cellular proliferation and enhanced apoptosis of myeloma cells. In primary samples, methylation of MIR34B/C occurred in 5.3% at diagnosis and 52.2% at relapse/disease progression (P < .001). In 12 MM patients with paired samples at diagnosis and relapse/progression, MIR34B/C methylation was acquired in 6 at relapse/progression. In conclusion, MIR34B/C is a tumor suppressor in myeloma. Hypermethylation of MIR34B/C is tumor-specific. Frequent MIR34B/C hypermethylation during relapse/progression but not at diagnosis implicated a role of MIR34B/C hypermethylation in myeloma relapse/progression. © 2011 by The American Society of Hematology.en_HK
dc.languageengen_US
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_HK
dc.relation.ispartofBlooden_HK
dc.subject.meshAzacitidine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshEpigenesis, Genetic - Drug Effects - Physiologyen_US
dc.subject.meshGene Expression Regulation, Neoplastic - Drug Effectsen_US
dc.subject.meshGene Silencing - Drug Effects - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMicrornas - Geneticsen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMultiple Myeloma - Genetics - Pathologyen_US
dc.subject.meshPrimary Cell Cultureen_US
dc.subject.meshRecurrenceen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleEpigenetic inactivation of the MIR34B/C in multiple myelomaen_HK
dc.typeArticleen_HK
dc.identifier.emailSo, CC:scc@pathology.hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.emailChim, CS:jcschim@hku.hken_HK
dc.identifier.authoritySo, CC=rp00391en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1182/blood-2011-06-361022en_HK
dc.identifier.pmid21976676en_HK
dc.identifier.scopuseid_2-s2.0-82155183260en_HK
dc.identifier.hkuros200868-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-82155183260&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume118en_HK
dc.identifier.issue22en_HK
dc.identifier.spage5901en_HK
dc.identifier.epage5904en_HK
dc.identifier.eissn1528-0020-
dc.identifier.isiWOS:000297576600030-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, KY=36151671200en_HK
dc.identifier.scopusauthoridYim, RLH=54781044700en_HK
dc.identifier.scopusauthoridSo, CC=7102919978en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK

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