Abstract
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.
Highlights
Adult T‐cell leukemia (ATL) is a highly aggressive malignant disease of CD4+ T cells, caused by human T‐cell lymphotropic virus type I (HTLV‐I) [1]
High mobility group box 1 (HMGB1) is an abundant and ubiquitous nuclear protein that binds to DNA and nucleosomes and induces structural changes in the chromatin fiber
The expression levels of HMGB1, receptor for advanced glycation end products (RAGE) (HMGB1 receptor) and Tax were analyzed by polymerase chain reaction (PCR) in eight HTLV‐I‐infected T‐cell lines [MT‐2, MT‐4, C5/MJ, SLB‐1, HuT‐102, MT‐1, TL‐OmI and ED‐40515(‐)]
Summary
Adult T‐cell leukemia (ATL) is a highly aggressive malignant disease of CD4+ T cells, caused by human T‐cell lymphotropic virus type I (HTLV‐I) [1]. The viral oncoprotein, plays a central role in tumorigenesis and contributes to the pathogenesis of ATL and inflammatory diseases by inducing persistent activation of numerous cellular transcription factors, including nuclear factor‐κB, cyclic adenosine 3',5'‐monophosphate response element‐binding protein and activator protein 1, leading to transactivation of cellular gene promoters [4]. High mobility group box 1 (HMGB1) is an abundant and ubiquitous nuclear protein that binds to DNA and nucleosomes and induces structural changes in the chromatin fiber. It regulates numerous cellular activities, including transcription, replication and repair [5]. The levels HMGB1 in several T-cell lines and in the plasma of patients with ATL were analyzed
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