ArticlePloS one2013
The IKK inhibitor Bay 11-7082 induces cell death independent from inhibition of activation of NFκB transcription factors.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 71 citations in OpenAlex.
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- Maintenance of X chromosome inactivation after T cell activation requires NF-κB signaling.Science immunology · 2024Article
- Platelet transcription factors license the pro-inflammatory cytokine response of human monocytes.EMBO molecular medicine · 2024Article
- In Vivo Effects of Bay 11-7082 on Fibroid Growth and Gene Expression: A Preclinical Study.Cells · 2024Article
- Metabolic rewiring of macrophages by epidermal-derived lactate promotes sterile inflammation in the murine skin.The EMBO journal · 2024Article
- Multiple approaches to repurposing drugs for neuroblastoma.Bioorganic & medicinal chemistry · 2022Article
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- Ethyl P-Methoxycinnamate: An Active Anti-Metastasis Agent and Chemosensitizer Targeting NFκB fromLife (Basel, Switzerland) · 2022Article
- Neutrophil DREAM promotes neutrophil recruitment in vascular inflammation.The Journal of experimental medicine · 2022Article
- Article
- NLRP3 Inflammasome Inhibitor BAY-117082 Reduces Oral Squamous Cell Carcinoma Progression.International journal of molecular sciences · 2021Article
- The inflammatory kinase IKKα phosphorylates and stabilizes c-Myc and enhances its activity.Molecular cancer · 2021Article
- Development of a human primary gut-on-a-chip to model inflammatory processes.Scientific reports · 2020Article
- Modulation of NLRP3 Inflammasome Attenuated Inflammatory Response Associated to Diarrhea-Predominant Irritable Bowel Syndrome.Biomedicines · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) displays an NFκB activity-related gene expression signature and about 20% of primary MM samples harbor genetic alterations conducive to intrinsic NFκB signaling activation. The relevance of blocking the classical versus the alternative NFκB signaling pathway and the molecular execution mechanisms involved, however, are still poorly understood. Here, we comparatively tested NFκB activity abrogation through TPCA-1 (an IKK2 inhibitor), BAY 11-7082 (an IKK inhibitor poorly selective for IKK1 and IKK2), and MLN4924 (an NEDD8 activating enzyme (NAE)-inhibitor), and analyzed their anti-MM activity. Whereas TPCA-1 interfered selectively with activation of the classical NFκB pathway, the other two compounds inhibited classical and alternative NFκB signaling without significant discrimination. Noteworthy, whereas TPCA-1 and MLN4924 elicited rather mild anti-MM effects with slight to moderate cell death induction after 1 day BAY 11-7082 was uniformly highly toxic to MM cell lines and primary MM cells. Treatment with BAY 11-7082 induced rapid cell swelling and its initial effects were blocked by necrostatin-1 or the ROS scavenger BHA, but a lasting protective effect was not achieved even with additional blockade of caspases. Because MLN4924 inhibits the alternative NFκB pathway downstream of IKK1 at the level of p100 processing, the quite discordant effects between MLN4924 and BAY 11-7082 must thus be due to blockade of IKK1-mediated NFκB-independent necrosis-inhibitory functions or represent an off-target effect of BAY 11-7082. In accordance with the latter, we further observed that concomitant knockdown of IKK1 and IKK2 did not have any major short-term adverse effect on the viability of MM cells.
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