HTLV-1 bZIP factor supports proliferation of adult T cell leukemia cells through suppression of C/EBPα signaling.
- Publisher:
- BioMed Central
- Publication Type:
- Journal Article
- Citation:
- Retrovirology, 2013, 10 pp. 1 - 13
- Issue Date:
- 2013-12-21
Open Access
Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Zhao, T | en_US |
dc.contributor.author | Coutts, A | en_US |
dc.contributor.author | Xu, L | en_US |
dc.contributor.author | Yu, J | en_US |
dc.contributor.author | Ohshima, K | en_US |
dc.contributor.author | Matsuoka, M | en_US |
dc.date.accessioned | 2017-09-18T05:57:30Z | |
dc.date.available | 2013-12-11 | en_US |
dc.date.available | 2017-09-18T05:57:30Z | |
dc.date.issued | 2013-12-21 | en_US |
dc.identifier.citation | Retrovirology, 2013, 10 pp. 1 - 13 | en_US |
dc.identifier.issn | 1742-4690 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/117262 | |
dc.description.abstract | BACKGROUND: Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus etiologically associated with adult T-cell leukemia (ATL). The HTLV-1 bZIP factor (HBZ), which is encoded by minus strand of provirus, is expressed in all ATL cases and supports the proliferation of ATL cells. However, the precise mechanism of growth promoting activity of HBZ is poorly understood. RESULTS: In this study, we showed that HBZ suppressed C/EBPα signaling activation induced by either Tax or C/EBPα. As mechanisms of HBZ-mediated C/EBPα inhibition, we found that HBZ physically interacted with C/EBPα and diminished its DNA binding capacity. Luciferase and immunoprecipitation assays revealed that HBZ repressed C/EBPα activation in a Smad3-dependent manner. In addition, C/EBPα was overexpressed in HTLV-1 infected cell lines and fresh ATL cases. HBZ was able to induce C/EBPα transcription by enhancing its promoter activity. Finally, HBZ selectively modulated the expression of C/EBPα target genes, leading to the impairment of C/EBPα-mediated cell growth suppression. CONCLUSION: HBZ, by suppressing C/EBPα signaling, supports the proliferation of HTLV-1 infected cells, which is thought to be critical for oncogenesis. | en_US |
dc.format | Electronic | en_US |
dc.language | eng | en_US |
dc.publisher | BioMed Central | en_US |
dc.relation.ispartof | Retrovirology | en_US |
dc.relation.isbasedon | 10.1186/1742-4690-10-159 | en_US |
dc.subject.classification | Virology | en_US |
dc.subject.mesh | T-Lymphocytes | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Human T-lymphotropic virus 1 | en_US |
dc.subject.mesh | CCAAT-Enhancer-Binding Protein-alpha | en_US |
dc.subject.mesh | Viral Proteins | en_US |
dc.subject.mesh | DNA | en_US |
dc.subject.mesh | Cell Proliferation | en_US |
dc.subject.mesh | Protein Binding | en_US |
dc.subject.mesh | Adult | en_US |
dc.subject.mesh | Aged | en_US |
dc.subject.mesh | Middle Aged | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Basic-Leucine Zipper Transcription Factors | en_US |
dc.subject.mesh | Host-Pathogen Interactions | en_US |
dc.subject.mesh | Adult | en_US |
dc.subject.mesh | Aged | en_US |
dc.subject.mesh | Basic-Leucine Zipper Transcription Factors | en_US |
dc.subject.mesh | CCAAT-Enhancer-Binding Protein-alpha | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Cell Proliferation | en_US |
dc.subject.mesh | DNA | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Host-Pathogen Interactions | en_US |
dc.subject.mesh | Human T-lymphotropic virus 1 | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Middle Aged | en_US |
dc.subject.mesh | Protein Binding | en_US |
dc.subject.mesh | Retroviridae Proteins | en_US |
dc.subject.mesh | T-Lymphocytes | en_US |
dc.subject.mesh | Viral Proteins | en_US |
dc.title | HTLV-1 bZIP factor supports proliferation of adult T cell leukemia cells through suppression of C/EBPα signaling. | en_US |
dc.type | Journal Article | |
utslib.description.version | Published | en_US |
utslib.citation.volume | 10 | en_US |
utslib.for | 1103 Clinical Sciences | en_US |
utslib.for | 1103 Clinical Sciences | en_US |
pubs.embargo.period | Not known | en_US |
utslib.copyright.status | open_access | |
pubs.declined | 2017-09-18T15:57:30.598+1000 | |
pubs.consider-herdc | false | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 10 | en_US |
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HTLV-1 bZIP factor supports proliferation of adult T cell leukemia cells through suppression of C/EBPα signaling.pdf | Published Version | 1.22 MB | Adobe PDF |
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Abstract:
BACKGROUND: Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus etiologically associated with adult T-cell leukemia (ATL). The HTLV-1 bZIP factor (HBZ), which is encoded by minus strand of provirus, is expressed in all ATL cases and supports the proliferation of ATL cells. However, the precise mechanism of growth promoting activity of HBZ is poorly understood. RESULTS: In this study, we showed that HBZ suppressed C/EBPα signaling activation induced by either Tax or C/EBPα. As mechanisms of HBZ-mediated C/EBPα inhibition, we found that HBZ physically interacted with C/EBPα and diminished its DNA binding capacity. Luciferase and immunoprecipitation assays revealed that HBZ repressed C/EBPα activation in a Smad3-dependent manner. In addition, C/EBPα was overexpressed in HTLV-1 infected cell lines and fresh ATL cases. HBZ was able to induce C/EBPα transcription by enhancing its promoter activity. Finally, HBZ selectively modulated the expression of C/EBPα target genes, leading to the impairment of C/EBPα-mediated cell growth suppression. CONCLUSION: HBZ, by suppressing C/EBPα signaling, supports the proliferation of HTLV-1 infected cells, which is thought to be critical for oncogenesis.
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