Loss of interleukin-2-dependency in HTLV-I-infected T cells on gene silencing of thioredoxin-binding protein-2

Ahsan, Md. Kaimul; Masutani, Hiroshi; Yamaguchi, Yuji; Kim, Y. C.; Nosaka, Kisato; Matsuoka, Masao; Nishinaka, Yumiko; Maeda, Masako; Yodoi, Junji

doi:10.1038/sj.onc.1209256

Cited by 60 publications

(47 citation statements)

References 25 publications

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“…4 Particularly, in view of the hypothesis that hyperglycemia may favor the cytotoxicity of certain drugs with similar suberoyalinide hydroxamic acid -mediated effects on TXNIP, the availability of compounds, such as 3-O-methylglucose, that stimulate TXNIP expression without being metabolized through phosphorylation by glucokinase, makes it attractive in terms of combining it with such drugs in preclinical animal models (42,43).…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia-Induced Thioredoxin-Interacting Protein Expression Differs in Breast Cancer–Derived Cells and Regulates Paclitaxel IC50

Turturro

Burton²,

Friday

2007

Clinical Cancer Research

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Purpose: We studied the hyperglycemia-induced expression of thioredoxin-interacting protein (TXNIP) expression and its relevance on the cytotoxic activity of paclitaxel in mammary epithelial^derived cell lines. Experimental Design: Nontumorigenic cells (MCF10A); tumorigenic, nonmetastatic cells (MCF-7/T47D); and tumorigenic, metastatic cells (MDA-MB-231/MDA-MB-435s) were grown either in 5 or 20 mmol/L glucose chronically. Semiquantitative reverse transcription-PCR was used to assess TXNIP RNA expression in response to glucose. Reactive oxygen species were detected by CM-H2DCFDA (5-6-chloromethyl-2 ¶,7 ¶-dichlorodihydrofluorescein diacetate) and measured for mean fluorescence intensity with flow cytometry. Thioredoxin activity was assayed by the insulin disulfide-reducing assay. Proliferation was evaluated using CellTiter96 reagent with 490-nm absorption. Obtained absorbance values were used to calculate the paclitaxel IC 50 in 5 or 20 mmol/L glucose using the Chou's dose-effect equation. Results: We show that hyperglycemia by itself affects the level of TXNIP RNA in breast cancerd erived cells. TXNIP RNA level differs between nontumorigenic/nonmetastatic, tumorigenic cells (low TXNIP level), and metastatic cells (highTXNIP level). The differences inTXNIP RNA level, in reactive oxygen species level, and in thioredoxin activity are all related. We further show that hyperglycemia is a favorable condition in increasing the paclitaxel cytotoxicity by causing IC 50 3-fold decrease in metastatic breast cancer^derived MDA-MB-231cells.The increased paclitaxel cytotoxicity is associated with an additive effect on the hyperglycemia-mediated TXNIP expression more evident in conditions of hyperglycemia than normoglycemia. Conclusions: Our study opens a new perspective on the relevance of metabolic conditions of hyperglycemia in the biology and treatment of cancer, particularly in view of the epidemic of diabetes.We have recently shown that the level of thioredoxininteracting protein (TXNIP) RNA, also known as vitamin D 3 up-regulated protein-1, statistically significantly increased in response to levels of glucose shifted from 5 mmol/L (equivalent to metabolic condition of normoglycemia) to 20 mmol/L (equivalent to conditions of diabetes or postprandial hyperglycemia) in the highly metastatic breast cancer -derived MDA-MD-231 cells grown in vitro tissue culture (1). We also showed that TXNIP RNA level corresponded to persistent elevation of TXNIP protein (e.g., ref. 1). 3 Although increased TXNIP RNA level induced by hyperglycemia (20 mmol/L glucose) was associated with unchanged thioredoxin RNA level, thioredoxin measurable activity was notably reduced (1.6-fold than the control), and the level of reactive oxygen species (ROS) increased (2.3-fold than control), in MDA-MD-231 cells (1). We further showed that glucose-induced TXNIP/thioredoxin/ ROS axis regulation was mediated by p38 mitogen-activated protein kinase (MAPK) signaling pathway because the use of SB203580-specific kinase inhibitor eliminated the glucosei...

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Section: Discussionmentioning

confidence: 99%

Hyperglycemia-Induced Thioredoxin-Interacting Protein Expression Differs in Breast Cancer–Derived Cells and Regulates Paclitaxel IC50

Turturro

Burton²,

Friday

2007

Clinical Cancer Research

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“…A key selenoenzyme in mediating these effects may be Txnrd1, which produces higher levels of reduced Txn-1 in CD4 + T cells from Se supplemented mice (102). Txnrd1 converts oxidized Txn-1 to reduced Txn-1 in the cytoplasm and nucleus, which is important because Txn-1 has been linked to regulation of H3K9 tri-methylation and -acetylation and to production of the cytokine, IL-2, which is involved in T cell proliferation and Th1 differentiation (2,195). Thus, free thiols and Txn-1 as well as other redox intermediates may represent important mechanisms by which Se supplementation affects epigenetic events in naive CD4 + T cells.…”

Section: Fig 11 Analyses Of Cell Markers During Activation Of Naivementioning

confidence: 99%

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

Huang

Rose

Hoffmann

2012

Antioxidants & Redox Signaling

710

496

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Dietary selenium (]Se), mainly through its incorporation into selenoproteins, plays an important role in inflammation and immunity. Adequate levels of Se are important for initiating immunity, but they are also involved in regulating excessive immune responses and chronic inflammation. Evidence has emerged regarding roles for individual selenoproteins in regulating inflammation and immunity, and this has provided important insight into mechanisms by which Se influences these processes. Se deficiency has long been recognized to negatively impact immune cells during activation, differentiation, and proliferation. This is related to increased oxidative stress, but additional functions such as protein folding and calcium flux may also be impaired in immune cells under Se deficient conditions. Supplementing diets with above-adequate levels of Se can also impinge on immune cell function, with some types of inflammation and immunity particularly affected and sexually dimorphic effects of Se levels in some cases. In this comprehensivearticle, the roles of Se and individual selenoproteins in regulating immune cell signaling and function are discussed. Particular emphasis is given to how Se and selenoproteins are linked to redox signaling, oxidative burst, calcium flux, and the subsequent effector functions of immune cells. Data obtained from cell culture and animal models are reviewed and compared with those involving human physiology and pathophysiology, including the effects of Se levels on inflammatory or immune-related diseases including anti-viral immunity, autoimmunity, sepsis, allergic asthma, and chronic inflammatory disorders. Finally, the benefits and potential adverse effects of intervention with Se supplementation for various inflammatory or immune disorders are discussed. Antioxid. Redox Signal. 16, 705-743.

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“…The expression of TBP2 is lost in HTLV-I-positive, interleukin-2-independent T cell lines but maintained in HTLV-I-positive, interleukin-2-dependent T cell lines, as well as HTLVI-negative T cell lines (25,26). Ectopic overexpression of TBP2 in HTLV-I-positive T cells resulted in growth suppression.…”

Section: Trx Binding Proteinmentioning

confidence: 99%

Thioredoxin and thioredoxin binding protein 2 in the liver

et al. 2008

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SummaryThioredoxin (TRX) is a 12-kDa protein with redox-active dithiol in the active site -Cys-Gly-Pro-Cys-and constitutes a major thiol reducing system. TRX protects cells from stressinduced damage through antioxidative, antiapoptotic, and antiinflammatory effect. In animal models, thioacetamide (TAA)-induced acute hepatitis and TAA-induced liver fibrosis was attenuated in TRX transgenic (TRXTG) mice. Plasma level of TRX is a good marker for hepatitis and nonalcoholic steatohepatitis (NASH) in human patients. Recently, we identified TRX binding protein 2 (TBP2) in a yeast two-hybrid screening. TBP2 regulates both the expression and reducing activity of TRX as well as cell growth. TBP2 knockout (TBP2KO) mice showed disorder in lipid metabolism. TBP2 plays a multiple role on cell growth and lipid and glucose metabolism. Thus, TRX and TBP2 play important roles in the pathophysiology of liver diseases, including NASH, indicating that ratio of TRX and TBP2 expression could be a novel marker of liver diseases like NASH.2008 IUBMB IUBMB Life, 60(10): 656-660, 2008

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Loss of interleukin-2-dependency in HTLV-I-infected T cells on gene silencing of thioredoxin-binding protein-2

Cited by 60 publications

References 25 publications

Hyperglycemia-Induced Thioredoxin-Interacting Protein Expression Differs in Breast Cancer–Derived Cells and Regulates Paclitaxel IC50

Hyperglycemia-Induced Thioredoxin-Interacting Protein Expression Differs in Breast Cancer–Derived Cells and Regulates Paclitaxel IC50

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

Thioredoxin and thioredoxin binding protein 2 in the liver

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