Article: Epigenetic inactivation of the MIR34B/C in multiple myeloma
| Title | Epigenetic inactivation of the MIR34B/C in multiple myeloma | ||||
|---|---|---|---|---|---|
| Authors | Wong, KY1 Yim, RLH1 So, CC1 Jin, DY1 Liang, R1 Chim, CS1 | ||||
| Issue Date | 2011 | ||||
| Publisher | American 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?] DOI: http://dx.doi.org/10.1182/blood-2011-06-361022 | ||||
| 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. | ||||
| ISSN | 0006-4971 2011 Impact Factor: 9.898 2011 SCImago Journal Rankings: 1.698 | ||||
| DOI | http://dx.doi.org/10.1182/blood-2011-06-361022 | ||||
| ISI Accession Number ID | WOS:000297576600030
Funding Information: This work was supported by the Hong Kong Research Grants Council General Research Fund (#763409M). | ||||
| References | References in Scopus |
| dc.contributor.author | Wong, KY | ||||
|---|---|---|---|---|---|
| dc.contributor.author | Yim, RLH | ||||
| dc.contributor.author | So, CC | ||||
| dc.contributor.author | Jin, DY | ||||
| dc.contributor.author | Liang, R | ||||
| dc.contributor.author | Chim, CS | ||||
| dc.date.accessioned | 2012-05-29T06:14:30Z | ||||
| dc.date.available | 2012-05-29T06:14:30Z | ||||
| dc.date.issued | 2011 | ||||
| dc.description.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. | ||||
| dc.description.nature | Link_to_subscribed_fulltext | ||||
| dc.identifier.citation | Blood, 2011, v. 118 n. 22, p. 5901-5904 [How to Cite?] DOI: http://dx.doi.org/10.1182/blood-2011-06-361022 | ||||
| dc.identifier.doi | http://dx.doi.org/10.1182/blood-2011-06-361022 | ||||
| dc.identifier.epage | 5904 | ||||
| dc.identifier.hkuros | 200868 | ||||
| dc.identifier.isi | WOS:000297576600030
Funding Information: This work was supported by the Hong Kong Research Grants Council General Research Fund (#763409M). | ||||
| dc.identifier.issn | 0006-4971 2011 Impact Factor: 9.898 2011 SCImago Journal Rankings: 1.698 | ||||
| dc.identifier.issue | 22 | ||||
| dc.identifier.pmid | 21976676 | ||||
| dc.identifier.scopus | eid_2-s2.0-82155183260 | ||||
| dc.identifier.spage | 5901 | ||||
| dc.identifier.uri | http://hdl.handle.net/10722/148661 | ||||
| dc.identifier.volume | 118 | ||||
| dc.language | eng | ||||
| dc.publisher | American Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/ | ||||
| dc.publisher.place | United States | ||||
| dc.relation.ispartof | Blood | ||||
| dc.relation.references | References in Scopus | ||||
| dc.subject.mesh | Azacitidine - Analogs & Derivatives - Pharmacology | ||||
| dc.subject.mesh | Base Sequence | ||||
| dc.subject.mesh | Dna Methylation | ||||
| dc.subject.mesh | Disease Progression | ||||
| dc.subject.mesh | Epigenesis, Genetic - Drug Effects - Physiology | ||||
| dc.subject.mesh | Gene Expression Regulation, Neoplastic - Drug Effects | ||||
| dc.subject.mesh | Gene Silencing - Drug Effects - Physiology | ||||
| dc.subject.mesh | Humans | ||||
| dc.subject.mesh | Micrornas - Genetics | ||||
| dc.subject.mesh | Molecular Sequence Data | ||||
| dc.subject.mesh | Multiple Myeloma - Genetics - Pathology | ||||
| dc.subject.mesh | Primary Cell Culture | ||||
| dc.subject.mesh | Recurrence | ||||
| dc.subject.mesh | Tumor Cells, Cultured | ||||
| dc.title | Epigenetic inactivation of the MIR34B/C in multiple myeloma | ||||
| dc.type | Article |
Author Affiliations
- The University of Hong Kong