NF-κB2/p100 induces Bcl-2 expression

Viatour, Patrick; Bentires‐Alj, Mohamed; Chariot, Alain; Deregowski, Valérie; Leval, Laurence de; Merville, Marie Paule; Bours, Vincent

doi:10.1038/sj.leu.2402982

Cited by 151 publications

(111 citation statements)

References 61 publications

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“…These data are supported by several other observations: 1) lymphoma cells with the t(14;18) translocation show high levels of NF-κB [15] and 2) in breast cancer and leukemic (CLL) cells high NF-κB expression was associated with high Bcl-2 expression [48]. In fact, it has been shown for MCF-7 breast cancer cells that Bcl-2 overexpression enhances NF-κB activity and induces MMP-9 transcription [32].…”

Section: Discussionsupporting

confidence: 77%

Helenalin bypasses Bcl-2-mediated cell death resistance by inhibiting NF-κB and promoting reactive oxygen species generation

Hoffmann

Schwarzenberg

López-Antón

et al. 2011

Biochemical Pharmacology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractEvasion of cell death by overexpression of anti-apoptotic proteins, such as Bcl-2, is commonly observed in cancer cells leading to a lack of response to chemotherapy.Hence, there is a need to find new chemotherapeutic agents that are able to overcome chemoresistance mediated by Bcl-2 and to understand their mechanisms of action. Helenalin, a sesquiterpene lactone ( and free intracellular iron as mediators of helenalin-induced cell death whereas activation of JNK and abrogation of Akt activity did not contribute to helenalin-elicited cell death. Our results highlight the NF-κB inhibitor helenalin as a promising chemotherapeutic agent to overcome Bcl-2-induced cell death resistance.

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Section: Discussionsupporting

confidence: 77%

Helenalin bypasses Bcl-2-mediated cell death resistance by inhibiting NF-κB and promoting reactive oxygen species generation

Hoffmann

Schwarzenberg

López-Antón

et al. 2011

Biochemical Pharmacology

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“…In agreement with this notion, the discernible defects in splenic architecture and generation and maintenance of germinal centers that characterize the p100 NF-kB2 knockout mice do not occur in animals lacking p105 NF-kB1 (Caamano et al, 1998;Franzoso et al, 1998). Recent studies also suggest a specific role for p52 as an antiapoptotic protein capable of inducing the expression of Bcl-2 Viatour et al, 2003) and highlight its physiological contribution to early transitional IgM þ /CD21 À B-cell survival (Claudio et al, 2002). Interestingly, LMP1 induces the expression of this antiapoptotic protein in lymphoid cells (Henderson et al, 1991) and this effect may be under the control of the p100 NF-kB2 pathway.…”

Section: Discussionsupporting

confidence: 53%

Epstein–Barr virus-encoded latent infection membrane protein 1 regulates the processing of p100 NF-κB2 to p52 via an IKKγ/NEMO-independent signalling pathway

et al. 2003

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The oncogenic Epstein-Barr virus (EBV)-encoded latent infection membrane protein 1 (LMP1) constitutively activates the 'canonical' NF-jB pathway that involves the phosphorylation and degradation of IjBa downstream of the IjB kinases (IKKs). In this study, we show that LMP1 also promotes the proteasome-mediated proteolysis of p100 NF-jB2 resulting in the generation of active p52, which translocates to the nucleus in complex with the p65 and RelB NF-jB subunits. LMP1-induced NF-jB transactivation is reduced in nf-kb2 À/À mouse embryo fibroblasts, suggesting that p100 processing contributes to LMP1-mediated NF-jB transcriptional effects. This pathway is likely to operate in vivo, as the expression of LMP1 in primary EBV-positive Hodgkin's lymphoma and nasopharyngeal carcinoma biopsies correlates with the nuclear accumulation of p52. Interestingly, while the ability of LMP1 to activate the canonical NF-jB pathway is impaired in cells lacking IKKc/NEMO, the regulatory subunit of the IKK complex, p100 processing remains unaffected. As a result, nuclear translocation of p52, but not p65, occurs in the absence of IKKc. These data point to the existence of a novel signalling pathway that regulates NF-jB in LMP1-expressing cells, and may thereby play a role in both oncogenic transformation and the establishment of persistent EBV infection.

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“…Regulation of the classical and alternative NF-κB activation is important because the activation of these two NF-κB pathways result in functionally distinct outcomes for the cell. The classical NF-κB pathway is involved in cellular activation [45], whereas the alternative pathway is linked to the initiation of pro-cell survival pathways [46] and in lymphatic tissue development [47].…”

Section: Cd27mentioning

confidence: 99%

Roles of TRAF molecules in B lymphocyte function

Xie

Kraus

Stunz

et al. 2008

Cytokine & Growth Factor Reviews

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Tumor necrosis factor receptor associated factors (TRAFs) play a variety of interesting and important roles in the regulation of B lymphocyte function. They act both as cytoplasmic regulatory molecules, and as signal transducers for receptors involved in both innate and adaptive humoral immune responses. In this brief review, we highlight the current state of knowledge of the diverse roles of TRAF molecules in the functions of B lymphocytes. CD40CD40 is the most well-studied member of the TNFR superfamily expressed by B lymphocytes, so its interactions with TRAF molecules have also been intensively investigated. B cell CD40 is important in the induction of B cell survival and expansion, immunoglobulin (Ig) production and isotype switching, upregulation of surface molecules involved in B cell antigen presentation, differentiation to B memory cells, and the production of various cytokines (reviewed in [1]. The TRAF molecules have been shown to contribute to each of these functions (reviewed in [2].In 1994, TRAF3 became the first cytoplasmic molecule demonstrated to associate with CD40 (reviewed in [2]). However, for many years, its roles in CD40 signaling were largely unknown, and are still not completely understood. TRAF3 -/-mice die shortly after birth, but adoptive transfer of fetal liver cells from these mice suggested that their B cells were capable of reconstituting the humoral response [3], implying that TRAF3 is not required to promote CD40-mediated antibody responses. This conclusion was supported by experiments in B cell lines demonstrating that inducible overexpression of TRAF3 inhibits both CD40 responses [4], and cooperation between CD40 and the BCR [5]. Subsequently, B cell lines made completely TRAF3-deficient via gene targeting by homologous recombination show no defects in CD40 signaling overall, and display enhanced CD40-mediated c-jun kinase (JNK) activation and IgM production [6]. Recently, mice made conditionally deficient in TRAF3 only in CD19+ B cells show no deficiencies in CD40 signaling in vitro and have enhanced antibody responses [7]. TRAF2 was initially demonstrated to bind CD40 by exogenous overexpression studies in adenocarcinoma cell lines, in which it promotes JNK activation and the activity of NF-κB reporter genes (reviewed in [2]. Because TRAF2 -/-mice have an early lethal phenotype [8],Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers

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NF-κB2/p100 induces Bcl-2 expression

Cited by 151 publications

References 61 publications

Helenalin bypasses Bcl-2-mediated cell death resistance by inhibiting NF-κB and promoting reactive oxygen species generation

Helenalin bypasses Bcl-2-mediated cell death resistance by inhibiting NF-κB and promoting reactive oxygen species generation

Epstein–Barr virus-encoded latent infection membrane protein 1 regulates the processing of p100 NF-κB2 to p52 via an IKKγ/NEMO-independent signalling pathway

Roles of TRAF molecules in B lymphocyte function

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