scholarly journals Hydrogen Sulfide Inhibits Human T-cell Leukemia Virus Type-1 (HTLV-1) Protein Expression via Regulation of ATG4B

2021 ◽  
Author(s):  
Liu Huandi ◽  
Jiaxiang Sun ◽  
Shuaifeng Guo ◽  
Xuhong Cheng ◽  
Zhongxin Zhang ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
T Cell ◽  
Protein Expression ◽  
Leukemia Virus ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
Pathway Activation ◽  
T Cell Leukemia Virus ◽  
T Cell Lines ◽  
High Level

Abstract Background: Hydrogen sulfide(H 2 S)is a redox gasotransmitter. It has been shown that H 2 S has a key role in host antiviral defense by inhibiting interleukin (IL)-6 production and S-sulfhydrating Keap1 lead to Nrf2/ARE pathway activation. However, it is yet unclear whether H 2 S can play an antiviral role by regulating autophagy. Results: In this research, we found that exogenous H 2 S decreased the expression of HTLV-1 protein and HTLV-1 induced autophagosomes accumulation. Transmission electron microscope assays indicated that autophagosomes accumulation decreased after H 2 S administration. HTLV-1-transformed T-cell lines had a high level of CSE (H 2 S endogenous enzyme) which could be induced in Hela by HTLV-1 infection. Immunoblot demonstrated that overexpression of CSE inhibited HTLV-1 protein expression and autophagy. And we got the opposite after CSE knockdown. Meanwhile, H 2 S could not restrain the autophagy when ATG4B had a mutant at its site of 89. Conclusion: In a word, these results suggested that H 2 S modulated HTLV-1 protein expression via ATG4B. Meanwhile, our findings suggested a new mechanism by which H 2 S defended against virus infection.

Enhanced expression of LFA-3 on human T-cell lines and leukemic cells carrying human T-cell-leukemia virus type 1

1993 ◽  
Vol 55 (5) ◽  
pp. 811-816 ◽  
Author(s):  
Toshio Imai ◽  
Yoshikazu Tanaka ◽  
Kenji Fukudome ◽  
Shin Takagi ◽  
Koichi Araki ◽  
...  
Keyword(s):  
T Cell ◽  
Leukemia Virus ◽  
Leukemic Cells ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Enhanced Expression ◽  
T Cell Lines

scholarly journals Homotypic Cell–Cell Adhesion Induced by Human T Cell Leukemia Virus Type 1 Tax Protein in T Cell Lines

Virology ◽  
2002 ◽  
Vol 302 (1) ◽  
pp. 132-143 ◽  
Author(s):  
Toshiyuki Takahashi ◽  
Masaya Higuchi ◽  
Masaya Fukushi ◽  
Masayasu Oie ◽  
Masaaki Ito ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
T Cell ◽  
Leukemia Virus ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Tax Protein ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
T Cell Lines

scholarly journals Human T-Cell Leukemia Virus Type 1 Tax Dysregulates β-CateninSignaling

2006 ◽  
Vol 80 (21) ◽  
pp. 10497-10505 ◽  
Author(s):  
Mariko Tomita ◽  
Akira Kikuchi ◽  
Tetsu Akiyama ◽  
Yuetsu Tanaka ◽  
Naoki Mori
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Glycogen Synthase ◽  
Leukemia Virus ◽  
Camp Response Element Binding ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Element Binding Protein ◽  
T Cell Lines

ABSTRACT Dysregulation of β-catenin signaling has been implicated in the malignant transformation of cells. However, the role of β-catenin in the human T-cell leukemia virus type 1 (HTLV-1)-induced transformation of T cells is unknown. Here we found that β-catenin protein was overexpressed in the nucleus and that β-catenin-dependent transcription was significantly enhanced in Tax-positive HTLV-1-infected T-cell lines compared to that in Tax-negative HTLV-1-infected T-cell lines. Transfection withβ -catenin-specific small interfering RNA inhibited the growth of the Tax-positive HTLV-1-infected T-cell line HUT-102. Transient transfection of Tax appeared to enhance β-catenin-dependent transcription by stabilizing the β-catenin protein via activation of the cyclic AMP (cAMP) response element-binding protein. HTLV-1-infected T-cell lines overexpressing β-catenin also showed increased Akt activity via Tax activation of the cAMP response element-binding protein, resulting in the phosphorylation and inactivation of glycogen synthase kinase 3β, which phosphorylates β-catenin for ubiquitination. The phosphatidylinositol 3-kinase inhibitor LY294002 reducedβ -catenin expression in Tax-positive T-cell lines, and inactivation of glycogen synthase kinase 3β by lithium chloride restored β-catenin expression in Tax-negative T-cell lines. Finally, we showed that dominant-negative Akt inhibited Tax-inducedβ -catenin-dependent transcription. These results indicate that Tax activates β-catenin through the Akt signaling pathway. Our findings suggest that activation of β-catenin by Tax may be important in the transformation of T cells by HTLV-1 infection.

scholarly journals Phosphoinositide-3 kinase-PKB/Akt pathway activation is involved in fibroblast Rat-1 transformation by human T-cell leukemia virus type I tax

Oncogene ◽  
2001 ◽  
Vol 20 (20) ◽  
pp. 2514-2526 ◽  
Author(s):  
Yan Liu ◽  
Yin Wang ◽  
Munekazu Yamakuchi ◽  
Satoko Masuda ◽  
Takeshi Tokioka ◽  
...  
Keyword(s):  
T Cell ◽  
Leukemia Virus ◽  
Akt Pathway ◽  
Type I ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
Pathway Activation ◽  
T Cell Leukemia Virus ◽  
Phosphoinositide 3 Kinase

scholarly journals Resistance to Apo2 Ligand (Apo2L)/Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-Mediated Apoptosis and Constitutive Expression of Apo2L/TRAIL in Human T-Cell Leukemia Virus Type 1-Infected T-Cell Lines

2005 ◽  
Vol 79 (3) ◽  
pp. 1367-1378 ◽  
Author(s):  
Takehiro Matsuda ◽  
Alex Almasan ◽  
Mariko Tomita ◽  
Jun-nosuke Uchihara ◽  
Masato Masuda ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Leukemia Virus ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Induced Apoptosis ◽  
T Cell Lines

ABSTRACT Adult T-cell leukemia (ATL), a CD4+-T-cell malignancy caused by human T-cell leukemia virus type 1 (HTLV-1), is difficult to cure, and novel treatments are urgently needed. Apo2 ligand (Apo2L; also tumor necrosis factor-related apoptosis-inducing ligand [TRAIL]) has been implicated in antitumor therapy. We found that HTLV-1-infected T-cell lines and primary ATL cells were more resistant to Apo2L-induced apoptosis than uninfected cells. Interestingly, HTLV-1-infected T-cell lines and primary ATL cells constitutively expressed Apo2L mRNA. Inducible expression of the viral oncoprotein Tax in a T-cell line up-regulated Apo2L mRNA. Analysis of the Apo2L promoter revealed that this gene is activated by Tax via the activation of NF-κB. The sensitivity to Apo2L was not correlated with expression levels of Apo2L receptors, intracellular regulators of apoptosis (FLICE-inhibitory protein and active Akt). NF-κB plays a crucial role in the pathogenesis and survival of ATL cells. The resistance to Apo2L-induced apoptosis was reversed by N-acetyl-l-leucinyl-l-leucinyl-l-norleucinal (LLnL), an NF-κB inhibitor. LLnL significantly induced the Apo2L receptors DR4 and DR5. Our results suggest that the constitutive activation of NF-κB is essential for Apo2L gene induction and protection against Apo2L-induced apoptosis and that suppression of NF-κB may be a useful adjunct in clinical use of Apo2L against ATL.

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