Detection of inducible nitric oxide synthase (iNOS) mRNA by RT-PCR in ATL patients and HTLV-I infected cell lines: clinical features and apoptosis by NOS inhibitor

Sawada, Takashi; Matsuzaki, Hiromitsu; Nagasaki, Akitoshi; Hata, Hiroyuki; Yoshida, Minoru; Matsuoka, Masao; Kuribayashi, N; Kimura, Tatsuya; Harada, Naoko; Takatsuki, Kiyoshi; Mitsuya, Hiroaki; Mori, Masataka

doi:10.1038/sj.leu.2401398

Cited by 19 publications

(13 citation statements)

References 32 publications

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“…Cultured human T cells have been shown to express two isoforms of NO synthase, inducible NO synthase and endothelial NO synthase (18), and addition of a NO synthase inhibitor induces apoptosis in primary T cell lymphoma cells (19). This supports the presence of a NO-dependent antiapoptotic mechanism in T cells.…”

Section: Resultsmentioning

confidence: 76%

Thioredoxin is required for S-nitrosation of procaspase-3 and the inhibition of apoptosis in Jurkat cells

Mitchell

Morton

Fernhoff

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

144

130

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Section: Resultsmentioning

confidence: 76%

Thioredoxin is required for S-nitrosation of procaspase-3 and the inhibition of apoptosis in Jurkat cells

Mitchell

Morton

Fernhoff

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

144

130

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“…Although only a limited number of patients was analyzed, these results suggest that NO may be involved in the invasive character of ATL cells. 76 The expression of the iNOS gene was confirmed in HTLV-I-infected T cell lines expressing the viral transactivator Tax by Mori et al 77 In addition, they showed that the transcriptional regulatory region of the hiNOS gene was activated by Tax in Jurkat, independently of NF-B. Furthermore, iNOS mRNA was detected in leukemic cells from ATL patients, implying that the expression of the hiNOS gene is involved in the pathogenesis of HTLV-I-associated diseases.…”

Section: Anti-apoptotic Effects Of Nomentioning

confidence: 94%

Mechanisms involved in the pro- and anti-apoptotic role of NO in human leukemia

2000

Leukemia

129

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“…In fact, Tax transgenic mouse model develop an ATLL like disease, and express high levels of TNFα, IL-1β, IL-6 and IFNγ, which participate in iNOS expression [140,142]. Moreover, we and others have demonstrated high levels of iNOS expression in HTLV-1 infected cells and this activation required the NF-kB pathway [87, 143,144].…”

Section: Regulation Of the Expression Of Inducible Nitric Oxide Synthmentioning

confidence: 99%

Contribution of Inducible Nitric Oxide Synthase to the Transformation of HTLV-1 Infected CD4+ T-Cells

Baydoun¹,

Ratner²

2015

J Leuk

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The Human T-cell Leukemia Virus type 1 (HTLV-1), is the first retrovirus associated with a human cancer. HTLV-1 is the causative agent of an aggressive and fatal malignancy of CD4+ T lymphocytes known as Adult T-cell Leukemia lymphoma (ATLL). Since the discovery of the virus in 1980, intensive investigations have been undertaken to determine how HTLV-1 drives the transformation process in infected cells. This is because the oncogenic features of HTLV-1 make it an excellent tool to dissect the molecular pathways involved in cancer development. More important, HTLV-1 induced leukemia is a typical inflammation-mediated malignancy with constitutive activation of the NF-kB pathway, which is also a critical determinant in many other cancers. How NF-kB contributes to the leukemogenic process is not completely defined. We recently demonstrated that the NF-kB pathway induces the expression of inducible nitric oxide synthase (iNOS) in HTLV-1 induced leukemia. iNOS enzymatically generates nitric oxide, which is an oxidative and nitrosative agent of DNA and proteins. Nitric oxide was found to be associated with a large number of DNA Double Strand Breaks (DSBs) in HTLV-1 transformed cells. Here, we will review the major effects of nitric oxide on HTLV-1 induced leukemia.

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Detection of inducible nitric oxide synthase (iNOS) mRNA by RT-PCR in ATL patients and HTLV-I infected cell lines: clinical features and apoptosis by NOS inhibitor

Cited by 19 publications

References 32 publications

Thioredoxin is required for S-nitrosation of procaspase-3 and the inhibition of apoptosis in Jurkat cells

Thioredoxin is required for S-nitrosation of procaspase-3 and the inhibition of apoptosis in Jurkat cells

Mechanisms involved in the pro- and anti-apoptotic role of NO in human leukemia

Contribution of Inducible Nitric Oxide Synthase to the Transformation of HTLV-1 Infected CD4+ T-Cells

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