Inhibition of EHMT2/G9a epigenetically increases the transcription of Beclin-1 via an increase in ROS and activation of NF-kappa B
DC Field | Value | Language |
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dc.contributor.author | Park, Sang Eun | - |
dc.contributor.author | Yi, Hye Jin | - |
dc.contributor.author | Suh, Nayoung | - |
dc.contributor.author | Park, Yun-Yong | - |
dc.contributor.author | Koh, Jae-Young | - |
dc.contributor.author | Jeong, Seong-Yun | - |
dc.contributor.author | Cho, Dong-Hyung | - |
dc.contributor.author | Kim, Choung-Soo | - |
dc.contributor.author | Hwang, Jung Jin | - |
dc.date.accessioned | 2021-08-11T17:26:05Z | - |
dc.date.available | 2021-08-11T17:26:05Z | - |
dc.date.issued | 2016-06-28 | - |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/9010 | - |
dc.description.abstract | We previously reported that BIX-01294 (BIX), a small molecular inhibitor of euchromatic histone-lysine N-methyltransferase 2 (EHMT2/G9a), induces reactive oxygen species (ROS)-dependent autophagy in MCF-7 cells. Herein, we analyzed the epigenetic mechanism that regulates the transcription of Beclin-1, a tumor suppressor and an autophagy-related gene (ATG). Inhibition of EHMT2 reduced dimethylation of lysine 9 on histone H3 (H3K9me2) and dissociated EHMT2 and H3K9me2 from the promoter of Beclin-1. To this promoter, RNA polymerase II and nuclear factor kappa B (NF-kappa B) were recruited in a ROS-dependent manner, resulting in transcriptional activation. Moreover, treatment with BIX reversed the suppression of Beclin-1 by the cooperative action of EHMT2 and DNA methyltransferase 1 (DNMT1). Accordingly, a combination treatment with BIX and 5-Aza-2'-deoxycytidine (5-Aza-Cd), a DNMT1 inhibitor, exerted a synergistic effect on Beclin-1 expression. Importantly, high levels of EHMT2 expression showed a significant association with low levels of Beclin-1 expression, which was related to a poor prognosis. These findings suggest that EHMT2 can directly repress Beclin-1 and that the inhibition of EHMT2 may be a useful therapeutic approach for cancer prevention by activating autophagy. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Impact Journals | - |
dc.title | Inhibition of EHMT2/G9a epigenetically increases the transcription of Beclin-1 via an increase in ROS and activation of NF-kappa B | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.18632/oncotarget.9290 | - |
dc.identifier.wosid | 000378614700065 | - |
dc.identifier.bibliographicCitation | Oncotarget, v.7, no.26, pp 39796 - 39808 | - |
dc.citation.title | Oncotarget | - |
dc.citation.volume | 7 | - |
dc.citation.number | 26 | - |
dc.citation.startPage | 39796 | - |
dc.citation.endPage | 39808 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | HISTONE METHYLTRANSFERASE G9A | - |
dc.subject.keywordPlus | MAMMALIAN-CELLS | - |
dc.subject.keywordPlus | DNA METHYLATION | - |
dc.subject.keywordPlus | AUTOPHAGY | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | 5-AZA-2'-DEOXYCYTIDINE | - |
dc.subject.keywordPlus | MACROAUTOPHAGY | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | ASSOCIATION | - |
dc.subject.keywordAuthor | EHMT2/G9a | - |
dc.subject.keywordAuthor | histone methyltransferase | - |
dc.subject.keywordAuthor | Beclin-1 | - |
dc.subject.keywordAuthor | autophagy | - |
dc.subject.keywordAuthor | epigenetic regulation | - |
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