Hostile takeovers: viral appropriation of the NF-kB pathway

Hiscott, John; Kwon, Hakju; Génin, Pierre

doi:10.1172/jci11918

Cited by 559 publications

(470 citation statements)

References 47 publications

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“…42 Unlike normal cells and tissues, constitutive activated NF-kB is detected in a wide variety of human cancer cells, and aberrant activation of NF-kB proteins is often associated with cellular transformation by various viral oncoproteins including Epstein-Barr virus latent membrane protein-1, hepatitis B virus X and hepatitis C virus core. 43 Particularly in lymphoid cells, a link between NF-kB activation and regulation of expression of Bcl-2 family proteins has been demonstrated. NF-kB was required for bcl-xl gene expression in T-cell lines, Jurkat and CTLL-2.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Kawakami

Tomita

Matsuda

et al. 2005

Intl Journal of Cancer

142

112

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Survivin, a unique member of the inhibitor of apoptosis protein family, is overexpressed in many cancers and considered to play an important role in oncogenesis. We previously reported the survivin expression profile in ATL, a CD4-positive T-cell malignancy caused by HTLV-I. HTLV-I Tax is thought to play an important role in immortalization of T cells. We have shown also that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by deprivation of IL-2 and converted its growth from being IL-2 dependent to being IL-2 independent through the NF-kB pathway. In our study, we demonstrate that constitutive expression of survivin was associated with resistance to apoptosis after IL-2 deprivation in Tax-expressing CTLL-2 cells. Transient transfection assays showed that survivin promoter was transactivated by Tax, via the activation of NF-kB. Pharmacological NFkB inhibition resulted in suppression of survivin expression and caused apoptosis of Tax-expressing CTLL-2 cells. Our findings suggest that activated NF-kB signaling contributes directly to malignant progression of ATL by preventing apoptosis, acting through the prosurvival protein survivin. ' 2005 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Kawakami

Tomita

Matsuda

et al. 2005

Intl Journal of Cancer

142

112

View full text Add to dashboard Cite

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“…NF-κB is activated by many viruses, including human immunodeficiency virus 1 (HIV-1), 37 human T cell leukemia virus-1, 38 hepatitis B virus, 39 hepatitis C virus (HCV), 40,41 Epstein Barr Virus, 42 rotavirus 43 and influenza virus 44 to promote viral replication, prevent virus-induced apoptosis, and mediate the immune response to the invading pathogen. 45 In contrast, activation of NF-κB by Sindbis 46,47 and Dengue virus 48 is associated with the induction of apoptosis, which may increase viral spread. In still other cases, proteins encoded by adenovirus, 49 HCV 50 and African swine fever virus 51 inhibit NF-κB activity to enhance replication or contribute to viral pathogenicity.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of NF-κ B activity and cFLIP expression contribute to viral-induced apoptosis

et al. 2005

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Virus-induced activation of nuclear factor-kappa B (NF-κB) is required for Type 3 (T3) reovirusinduced apoptosis. We now show that NF-κB is also activated by the prototypic Type 1 reovirus strain Lang (T1L), which induces significantly less apoptosis than T3 viruses, indicating that NF-κB activation alone is not sufficient for apoptosis in reovirus-infected cells. A second phase of virusinduced NF-κB regulation, where NF-κB activation is inhibited at later times following infection with T3 Abney (T3A), is absent in T1L-infected cells. This suggests that inhibition of NF-κB activation at later times post infection also contributes to reovirus-induced apoptosis. Reovirusinduced inhibition of stimulus-induced activation of NF-κB is significantly associated with apoptosis following infection of HEK293 cells with reassortant reoviruses and is determined by the T3 S1 gene segment, which is also the primary determinant of reovirus-induced apoptosis. Inhibition of stimulusinduced activation of NF-κB also occurs following infection of primary cardiac myocytes with apoptotic (8B) but not non-apoptotic (T1L) reoviruses. Expression levels of the NF-κB-regulated cellular FLICE inhibitory protein (cFLIP) reflect NF-κB activation in reovirus-infected cells. Further, inhibition of NF-κB activity and cFLIP expression promote T1L-induced apoptosis. These results demonstrate that inhibition of stimulus-induced activation of NF-κB and the resulting decrease in cFLIP expression promote reovirus-induced apoptosis.

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“…The proportion of cancer deaths attributable to these infectious agents has been estimated to range from 20% to 25% in developing countries and 7% to 10% in more industrialized countries (46). The first evidence implicating NF-B activation mediated pathogen-induced carcinogenesis was identification of the REV-T viral oncogene that causes avian reticuloendothelial lymphomatosis, v-Rel, which shares a Rel transactivation domain with the mammalian homologues NF-family members (47). Hepatitis B X protein and hepatitis C 5A and core proteins have been shown to activate NF-B and are implicated in carcinogenesis of hepatocellular carcinoma (48).…”

Section: Nf-b Links Inflammation To Cancermentioning

confidence: 99%

NF-κB Signaling Pathway, Inflammation and Colorectal Cancer

et al. 2009

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There is growing evidence for a connection between inflammation and tumor development, and the nuclear factor kappa B (NF-B), a proinflammatory transcription factor, is hypothesized to promote tumorigenesis. Although the genetic evidence for the hypothesis has been lacking, recent papers have lent credence to this hypothesis. It has been reported that constitutive NF-B activation in inflammatory bowel diseases (

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Hostile takeovers: viral appropriation of the NF-kB pathway

Cited by 559 publications

References 47 publications

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Inhibition of NF-κ B activity and cFLIP expression contribute to viral-induced apoptosis

NF-κB Signaling Pathway, Inflammation and Colorectal Cancer

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