Tax is Involved in Up-regulation of HMGB1 Expression Levels by Interaction with C/EBP

Zhang, Chenguang; Wang, Hui; ZhiGuo, Niu; Zhang, Jingjing; Yin, Ming-Mei; Zhi, Gao; Hu, Lihua

doi:10.7314/apjcp.2013.14.1.359

Cited by 6 publications

(8 citation statements)

References 34 publications

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“…In addition, Tax increased HMGB1 secretion in T cells. These results are consistent with those reported previously (11). Tax expression did not correlate with the upregulation of HMGB1 mRNA in HTLV-I-infected T-cell lines.…”

Section: Discussionsupporting

confidence: 94%

“…Thus, it plays an important role in cellular transformation (3,4). Recently, it has been reported that Tax is involved in upregulation of HMGB1 expression by interaction with CCAAT/enhancer binding protein (11). The present study found that HMGB1 mRNA was abundantly expressed in HTLV-I-infected T-cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…More recently, Zhang et al (11) have demonstrated that HMGB1 expression is upregulated by HTLV-I Tax in T cells. However, the expression levels of HMGB1 in HTLV-I-infected T-cell lines have not been determined.…”

Section: Introductionmentioning

confidence: 99%

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Abundant expression of HMGB1 in human T-cell lymphotropic virus type I-infected T-cell lines and high plasma levels of HMGB1 in patients with adult T-cell leukemia

Kimura

Mori

2014

Oncology Letters

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High mobility group box 1 (HMGB1) functions as a chromatin-associated nuclear protein and an extracellular signaling molecule. The concentration of HMGB1 protein and the expression of HMGB1 mRNA were analyzed by ELISA and polymerase chain reaction (PCR), respectively. The present study reports high plasma HMGB1 levels in patients with adult T-cell leukemia [ATL; which is caused by infection with human T-cell lymphotropic virus type I (HTLV-I)] compared with normal controls. In addition, HMGB1 was highly expressed in HTLV-I-infected T-cell lines compared with uninfected T-cell lines. The HTLV-I oncoprotein, Tax, induced extracellular release of HMGB1 in T cells. The results suggest that HMGB1 is a potential biomarker and a therapeutic target for ATL.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Abundant expression of HMGB1 in human T-cell lymphotropic virus type I-infected T-cell lines and high plasma levels of HMGB1 in patients with adult T-cell leukemia

Kimura

Mori

2014

Oncology Letters

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“…The results represent the means ±SD of triplicate determinations. One-way ANOVA; *, P < 0.05; **, P < 0.01. sequencing results confirmed that the PCR products corresponded to HMGB1 promoter sequence ( Figure 5E) [41].…”

Section: Pedv-n Is Enriched In the Hmgb1 Promotor And C/ebp Binding Msupporting

confidence: 55%

Porcine epidemic diarrhea virus nucleoprotein contributes to HMGB1 transcription and release by interacting with C/EBP-β

et al. 2016

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Porcine epidemic diarrhea is a devastating swine enteric disease, which is caused by porcine epidemic diarrhea virus (PEDV) infection. Our studies demonstrated that PEDV infection resulted in the up-regulation of proinflammatory cytokines. Meanwhile, PEDV infection and overexpression of viral nucleoprotein resulted in the acetylation and release of high mobility group box 1 proteins in vitro, an important proinflammatory response mediator, which contributes to the pathogenesis of various inflammatory diseases. Our studies also showed that SIRT1, histone acetyltransferase, and NF-κB regulated the acetylation and release of HMGB1. Chromatin immunoprecipitation, dual-luciferase reporter gene assay, and co-immunoprecipitation experiments illustrated that PEDV-N could induce HMGB1 transcription by interacting with C/EBP-β, which could bind to C/EBP motif in HMGB1 promotor region. Collectively, our data indicate PEDV-N contributes to HMGB1 transcription and the subsequent release/acetylation of HMGB1 during PEDV infection.

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“…Tax acts as a transcriptional activator by associating with specific DNA-bound protein and transcript factors. A recent study indicated that Tax can interact with C/EBPs in HMGB1 promoter and promote subsequent HMGB1 expression in CD4+ T-cells (Zhang et al, 2013b). These findings suggest that HMGB1 may be involved in HTLV-1-mediated adult T-cell leukemia.…”

Section: Hmgb1 Transcriptional Regulation (Figure 8)mentioning

confidence: 99%

HMGB1 in health and disease

Kang

Chen

Zhang

et al. 2014

Molecular Aspects of Medicine

822

828

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Complex genetic and physiological variations as well as environmental factors that drive emergence of chromosomal instability, development of unscheduled cell death, skewed differentiation, and altered metabolism are central to the pathogenesis of human diseases and disorders. Understanding the molecular bases for these processes is important for the development of new diagnostic biomarkers, and for identifying new therapeutic targets. In 1973, a group of non-histone nuclear proteins with high electrophoretic mobility was discovered and termed High-Mobility Group (HMG) proteins. The HMG proteins include three superfamilies termed HMGB, HMGN, and HMGA. High-mobility group box 1 (HMGB1), the most abundant and well-studied HMG protein, senses and coordinates the cellular stress response and plays a critical role not only inside of the cell as a DNA chaperone, chromosome guardian, autophagy sustainer, and protector from apoptotic cell death, but also outside the cell as the prototypic damage associated molecular pattern molecule (DAMP). This DAMP, in conjunction with other factors, thus has cytokine, chemokine, and growth factor activity, orchestrating the inflammatory and immune response. All of these characteristics make HMGB1 a critical molecular target in multiple human diseases including infectious diseases, ischemia, immune disorders, neurodegenerative diseases, metabolic disorders, and cancer. Indeed, a number of emergent strategies have been used to inhibit HMGB1 expression, release, and activity in vitro and in vivo. These include antibodies, peptide inhbitiors, RNAi, anti-coagulants, endogenous hormones, various chemical compounds, HMGB1-receptor and signaling pathway inhibition, artificial DNAs, physical strategies including vagus nerve stimulation and other surgical approaches. Future work further investigating the details of HMGB1 localizationtion, structure, post-translational modification, and identifccation of additional partners will undoubtedly uncover additional secrets regarding HMGB1’s multiple functions.

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Tax is Involved in Up-regulation of HMGB1 Expression Levels by Interaction with C/EBP

Cited by 6 publications

References 34 publications

Abundant expression of HMGB1 in human T-cell lymphotropic virus type I-infected T-cell lines and high plasma levels of HMGB1 in patients with adult T-cell leukemia

Abundant expression of HMGB1 in human T-cell lymphotropic virus type I-infected T-cell lines and high plasma levels of HMGB1 in patients with adult T-cell leukemia

Porcine epidemic diarrhea virus nucleoprotein contributes to HMGB1 transcription and release by interacting with C/EBP-β

HMGB1 in health and disease

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