Interleukin‐1β Induces Nuclear Factor κ B in Epithelial Cells Independently of the Production of Reactive Oxygen Intermediates

Bonizzi, Giuseppina; Dejardin, Emmanuel; Piret, Bernard; Piette, Jacques; Merville, Marie‐Paule; Bours, Vincent

doi:10.1111/j.1432-1033.1996.0544r.x

Cited by 86 publications

(66 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Since the redox status of di erent cell types may vary, it is possible that some of these e ects are cell type-dependent. In fact, distinct signal transduction pathways leading to NF-kB induction by IL-1 in epithelial and lymphoid cells have been observed (Bonizzi et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Overexpression of γ-glutamylcysteine synthetase suppresses tumor necrosis factor-induced apoptosis and activation of nuclear transcription factor-kappa B and activator protein-1

1999

View full text Add to dashboard Cite

Tumor necrosis factor (TNF) is a highly pleiotropic cytokine whose activity is at least partially regulated by the redox status of the cell. The cellular redox status is controlled primarily by glutathione, a major cellular antioxidant, whose synthesis is regulated by the ratelimiting enzyme g-glutamylcysteine synthetase (g-GCS).In the present report we investigated the e ect of g-GCS overexpression on the TNF-induced activation of nuclear transcription factors NF-kB and AP-1, stress-activated protein kinase/c-Jun amino-terminal kinase (JNK) and apoptosis. Transfection of cells with g-GCS cDNA blocked TNF-induced NF-kB activation, cytoplasmic IkBa degradation, nuclear translocation of p65, and NF-kB-dependent gene transcription. g-GCS overexpression also completely suppressed NF-kB activation induced by phorbol ester and okadaic acid, whereas that induced by H 2 O 2 , ceramide, and lipopolysaccharide was minimally a ected. g-GCS also abolished the activation of AP-1 induced by TNF and inhibited TNF-induced activation of JNK and mitogen-activated protein kinase kinase. TNF-mediated cytotoxicity and activation of caspase-3 were both abrogated in g-GCS-overexpressing cells. Overall, our results indicate that most of the pleiotropic actions of TNF are regulated by the glutathione-controlled redox status of the cell.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Di erent agents may activate NF-kB by di erent mechanisms (Suzuki et al, 1994;Bowie et al, 1997;Bonizzi et al, 1996). For instance NAC blocks TNF-and PMA-induced NF-kB but not that induced by okadaic acid (Suzuki et al, 1994).…”

Section: G-gcs Inhibits Nf-kb Activation Induced By a Wide Variety Ofmentioning

confidence: 99%

Overexpression of γ-glutamylcysteine synthetase suppresses tumor necrosis factor-induced apoptosis and activation of nuclear transcription factor-kappa B and activator protein-1

1999

View full text Add to dashboard Cite

show abstract

“…Inhibition of NF-B Activation by ␥-Tocotrienol Is Not Cell Type-specific-Distinct signal transduction pathways can mediate NF-B induction in different cell types (40,41). Therefore, besides myeloid cells, we investigated the effect of ␥-tocotrienol on TNF-induced NF-B activation in human epithelial H1299, A293, and MCF-7 cells (Fig.…”

Section: ␥-Tocotrienol Blocks Nf-b Activation Induced By Variousmentioning

confidence: 99%

γ-Tocotrienol Inhibits Nuclear Factor-κB Signaling Pathway through Inhibition of Receptor-interacting Protein and TAK1 Leading to Suppression of Antiapoptotic Gene Products and Potentiation of Apoptosis

Ahn

Sethi

Krishnan

et al. 2007

Journal of Biological Chemistry

233

205

View full text Add to dashboard Cite

Unlike the tocopherols, the tocotrienols, also members of the vitamin E family, have an unsaturated isoprenoid side chain. In contrast to extensive studies on tocopherol, very little is known about tocotrienol. Because the nuclear factor-B (NF-B) pathway has a central role in tumorigenesis, we investigated the effect of ␥-tocotrienol on the NF-B pathway. Although ␥-tocotrienol completely abolished tumor necrosis factor ␣ (TNF)-induced NF-B activation, a similar dose of ␥-tocopherol had no effect. Besides TNF, ␥-tocotrienol also abolished NF-B activation induced by phorbol myristate acetate, okadaic acid, lipopolysaccharide, cigarette smoke, interleukin-1␤, and epidermal growth factor. Constitutive NF-B activation expressed by certain tumor cells was also abrogated by ␥-tocotrienol. Reducing agent had no effect on the ␥-tocotrienol-

show abstract

“…Electrophoretic Mobility Shift Assays (EMSA) and supershifting analyses were performed as described (Bonizzi et al, 1996). The kB probes from the bax promoter are described in Figure 2.…”

Section: Electrophoretic Mobility Shift Assay (Emsa)mentioning

confidence: 99%

Inhibition of the NF-κB transcription factor increases Bax expression in cancer cell lines

et al. 2001

Self Cite

View full text Add to dashboard Cite

The NF-kB transcription factor has been shown to inhibit apoptosis in several experimental systems. We therefore investigated whether the expression of the Bax proapoptotic protein could be in¯uenced by NF-kB activity. Increased Bax protein expression was detected in HCT116, OVCAR-3 and MCF7 cells stably expressing a mutated unresponsive IkB-a inhibitory protein that blocks NF-kB activity. Northern blots showed that bax mRNA expression was increased as a consequence of mutated IkB-a expression in HCT116 cells. A careful examination of the human bax gene promoter sequence showed three putative binding sites for NF-kB, and the kB2 site at position -687 could indeed bind NF-kB complexes in vitro. Transient transfection of a bax promoter luciferase construct in HCT116 cells showed that NF-kB proteins could partially inhibit the transactivation of the bax promoter by p53. Mutations or deletions of the kB sites, including kB2, indicated that this NF-kB-dependent inhibitory e ect did not require NF-kB DNA-binding, and was thus an indirect e ect. However, cotransfection of expression vectors for several known cofactors failed to identify a competition between p53 and NF-kB for a transcription coactivator. Our ®ndings thus demonstrate for the ®rst time that NF-kB regulates, through an indirect pathway, the bax gene expression. Oncogene (2001) 20, 2805 ± 2813.

show abstract

Interleukin‐1β Induces Nuclear Factor κ B in Epithelial Cells Independently of the Production of Reactive Oxygen Intermediates

Cited by 86 publications

References 44 publications

Overexpression of γ-glutamylcysteine synthetase suppresses tumor necrosis factor-induced apoptosis and activation of nuclear transcription factor-kappa B and activator protein-1

Overexpression of γ-glutamylcysteine synthetase suppresses tumor necrosis factor-induced apoptosis and activation of nuclear transcription factor-kappa B and activator protein-1

γ-Tocotrienol Inhibits Nuclear Factor-κB Signaling Pathway through Inhibition of Receptor-interacting Protein and TAK1 Leading to Suppression of Antiapoptotic Gene Products and Potentiation of Apoptosis

Inhibition of the NF-κB transcription factor increases Bax expression in cancer cell lines

Contact Info

Product

Resources

About