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Article: A proof-of-concept study for the pathogenetic role of enhancer hypomethylation of MYBPHL in multiple myeloma

TitleA proof-of-concept study for the pathogenetic role of enhancer hypomethylation of MYBPHL in multiple myeloma
Authors
Issue Date2021
PublisherNature Research: Fully open access journals. The Journal's web site is located at http://www.nature.com/srep/index.html
Citation
Scientific Reports, 2021, v. 11 n. 1, p. article no. 7009 How to Cite?
AbstractEnhancer DNA methylation and expression of MYBPHL was studied in multiple myeloma (MM). By bisulfite genomic sequencing, among the three CpGs inside the MYBPHL enhancer, CpG1 was significantly hypomethylated in MM cell lines (6.7–50.0%) than normal plasma cells (37.5–75.0%) (P = 0.007), which was negatively correlated with qPCR-measured MYBPHL expression. In RPMI-8226 and WL-2 cells, bearing the highest CpG1 methylation, 5-azadC caused enhancer demethylation and expression of MYBPHL. In primary samples, higher CpG1 methylation was associated with lower MYBPHL expression. By luciferase assay, luciferase activity was enhanced by MYBPHL enhancer compared with empty vector control, but reduced by site-directed mutagenesis of each CpG. RNA-seq data of newly diagnosed MM patients showed that MYBPHL expression was associated with t(11;14). MOLP-8 cells carrying t(11;14) express the highest levels of MYBPHL, and its knockdown reduced cellular proliferation and increased cell death. Herein, as a proof-of-concept, our data demonstrated that the MYBPHL enhancer, particularly CpG1, was hypomethylated and associated with increased MYBPHL expression in MM, which was implicated in myelomagenesis.
Persistent Identifierhttp://hdl.handle.net/10722/307890
ISSN
2023 Impact Factor: 3.8
2023 SCImago Journal Rankings: 0.900
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWong, KY-
dc.contributor.authorMorgan, GJ-
dc.contributor.authorBoyle, EM-
dc.contributor.authorCheng, ASL-
dc.contributor.authorYip, KYL-
dc.contributor.authorChim, CS-
dc.date.accessioned2021-11-12T13:39:23Z-
dc.date.available2021-11-12T13:39:23Z-
dc.date.issued2021-
dc.identifier.citationScientific Reports, 2021, v. 11 n. 1, p. article no. 7009-
dc.identifier.issn2045-2322-
dc.identifier.urihttp://hdl.handle.net/10722/307890-
dc.description.abstractEnhancer DNA methylation and expression of MYBPHL was studied in multiple myeloma (MM). By bisulfite genomic sequencing, among the three CpGs inside the MYBPHL enhancer, CpG1 was significantly hypomethylated in MM cell lines (6.7–50.0%) than normal plasma cells (37.5–75.0%) (P = 0.007), which was negatively correlated with qPCR-measured MYBPHL expression. In RPMI-8226 and WL-2 cells, bearing the highest CpG1 methylation, 5-azadC caused enhancer demethylation and expression of MYBPHL. In primary samples, higher CpG1 methylation was associated with lower MYBPHL expression. By luciferase assay, luciferase activity was enhanced by MYBPHL enhancer compared with empty vector control, but reduced by site-directed mutagenesis of each CpG. RNA-seq data of newly diagnosed MM patients showed that MYBPHL expression was associated with t(11;14). MOLP-8 cells carrying t(11;14) express the highest levels of MYBPHL, and its knockdown reduced cellular proliferation and increased cell death. Herein, as a proof-of-concept, our data demonstrated that the MYBPHL enhancer, particularly CpG1, was hypomethylated and associated with increased MYBPHL expression in MM, which was implicated in myelomagenesis.-
dc.languageeng-
dc.publisherNature Research: Fully open access journals. The Journal's web site is located at http://www.nature.com/srep/index.html-
dc.relation.ispartofScientific Reports-
dc.rightsScientific Reports. Copyright © Nature Research: Fully open access journals.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleA proof-of-concept study for the pathogenetic role of enhancer hypomethylation of MYBPHL in multiple myeloma-
dc.typeArticle-
dc.identifier.emailChim, CS: jcschim@HKUCC-COM.hku.hk-
dc.identifier.authorityChim, CS=rp00408-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41598-021-86473-y-
dc.identifier.pmid33772052-
dc.identifier.pmcidPMC7997988-
dc.identifier.scopuseid_2-s2.0-85103604181-
dc.identifier.hkuros329778-
dc.identifier.volume11-
dc.identifier.issue1-
dc.identifier.spagearticle no. 7009-
dc.identifier.epagearticle no. 7009-
dc.identifier.isiWOS:000635234000028-
dc.publisher.placeUnited Kingdom-

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