ELL targets c-Myc for proteasomal degradation and suppresses tumour growth
Chen, Yu1; Zhou, Chi1; Ji, Wei1; Mei, Zhichao1; Hu, Bo1; Zhang, Wei1; Zhang, Dawei1; Wang, Jing1; Liu, Xing1; Ouyang, Gang1; Zhou, Jiangang1; Xiao, Wuhan1,2
2016-03-01
Source PublicationNATURE COMMUNICATIONS
ISSN2041-1723
Volume7
AbstractIncreasing evidence supports that ELL (eleven-nineteen lysine-rich leukaemia) is a key regulator of transcriptional elongation, but the physiological function of Ell in mammals remains elusive. Here we show that ELL functions as an E3 ubiquitin ligase and targets c-Myc for proteasomal degradation. In addition, we identify that UbcH8 serves as a ubiquitin-conjugating enzyme in this pathway. Cysteine 595 of ELL is an active site of the enzyme; its mutation to alanine (C595A) renders the protein unable to promote the ubiquitination and degradation of c-Myc. ELL-mediated c-Myc degradation inhibits c-Myc-dependent transcriptional activity and cell proliferation, and also suppresses c-Myc-dependent xenograft tumour growth. In contrast, the ELL(C595A) mutant not only loses the ability to inhibit cell proliferation and xenograft tumour growth, but also promotes tumour metastasis. Thus, our work reveals a previously unrecognized function for ELL as an E3 ubiquitin ligase for c-Myc and a potential tumour suppressor.
SubtypeArticle
DOI10.1038/ncomms11057
WOS HeadingsScience & Technology
Indexed BySCI
Funding OrganizationCAS Major Scientific and Technological Project(XDA08010208) ; CAS Major Scientific and Technological Project(XDA08010208) ; NSFC(31461163003) ; NSFC(31461163003) ; CAS Major Scientific and Technological Project(XDA08010208) ; CAS Major Scientific and Technological Project(XDA08010208) ; NSFC(31461163003) ; NSFC(31461163003)
Language英语
WOS Research AreaScience & Technology - Other Topics
WOS SubjectMultidisciplinary Sciences
WOS KeywordCALCIUM-BINDING PROTEIN ; II ELONGATION-FACTOR ; COLORECTAL-CANCER ; TRANSCRIPTIONAL ELONGATION ; METASTASIS FORMATION ; GENE-TRANSCRIPTION ; CELL-GROWTH ; HIV-1 TAT ; COMPLEX ; LEUKEMIA
WOS IDWOS:000372887800001
Funding OrganizationCAS Major Scientific and Technological Project(XDA08010208) ; CAS Major Scientific and Technological Project(XDA08010208) ; NSFC(31461163003) ; NSFC(31461163003) ; CAS Major Scientific and Technological Project(XDA08010208) ; CAS Major Scientific and Technological Project(XDA08010208) ; NSFC(31461163003) ; NSFC(31461163003)
Citation statistics
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/342005/27755
Collection藻类生物学及应用研究中心_水生生物分子与细胞生物学研究中心
Affiliation1.Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan 430072, Peoples R China
2.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Peoples R China
Recommended Citation
GB/T 7714
Chen, Yu,Zhou, Chi,Ji, Wei,et al. ELL targets c-Myc for proteasomal degradation and suppresses tumour growth[J]. NATURE COMMUNICATIONS,2016,7.
APA Chen, Yu.,Zhou, Chi.,Ji, Wei.,Mei, Zhichao.,Hu, Bo.,...&Xiao, Wuhan.(2016).ELL targets c-Myc for proteasomal degradation and suppresses tumour growth.NATURE COMMUNICATIONS,7.
MLA Chen, Yu,et al."ELL targets c-Myc for proteasomal degradation and suppresses tumour growth".NATURE COMMUNICATIONS 7(2016).
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