ArticleThe Journal of biological chemistry2010
Smac mimetic compounds potentiate interleukin-1beta-mediated cell death.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Astrocytes and the tumor microenvironment inflammatory state dictate the killing of glioblastoma cells by Smac mimetic compounds.Cell death & disease · 2024Article
- Review
- Estradiol/GPER affects the integrity of mammary duct-like structures in vitro.Scientific reports · 2020Article
- HTiP: High-Throughput Immunomodulator Phenotypic Screening Platform to Reveal IAP Antagonists as Anti-cancer Immune Enhancers.Cell chemical biology · 2019Article
- Combination of IAP Antagonists and TNF-α-Armed Oncolytic Viruses Induce Tumor Vascular Shutdown and Tumor Regression.Molecular therapy oncolytics · 2018Article
- Intracellular apoptotic pathways: a potential target for reducing joint damage in rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Review
- Selective replication of oncolytic virus M1 results in a bystander killing effect that is potentiated by Smac mimetics.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Oncolytic virus synergizes with Smac mimetic compounds to induce rhabdomyosarcoma cell death in a syngeneic murine model.Oncotarget · 2017Article
- USP11: A key regulator of cIAP2 stability and sensitivity to SMAC mimetics.Molecular & cellular oncology · 2016Article
- USP11-dependent selective cIAP2 deubiquitylation and stabilization determine sensitivity to Smac mimetics.Cell death and differentiation · 2015Article
- Small-molecule SMAC mimetics as new cancer therapeutics.Pharmacology & therapeutics · 2014Review
- Smac mimetics and innate immune stimuli synergize to promote tumor death.Nature biotechnology · 2014Article
- Loss of cIAP1 attenuates soleus muscle pathology and improves diaphragm function in mdx mice.Human molecular genetics · 2013Article
- LRIG1 modulates cancer cell sensitivity to Smac mimetics by regulating TNFα expression and receptor tyrosine kinase signaling.Cancer research · 2012Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Smac mimetic compounds (SMCs) potentiate TNFα-mediated cancer cell death by targeting the inhibitor of apoptosis (IAP) proteins. In addition to TNFα, the tumor microenvironment is exposed to a number of pro-inflammatory cytokines, including IL-1β. Here, we investigated the potential impact of IL-1β on SMC-mediated death of cancer cells. Synergy was seen in a subset of a diverse panel of 21 cancer cell lines to the combination of SMC and IL-1β treatment, which required IL-1β-induced activation of the NF-κB pathway. Elevated NF-κB activity resulted in the production of TNFα, which led to apoptosis dependent on caspase-8 and RIP1. In addition, concurrent silencing of cIAP1, cIAP2, and X-linked IAP by siRNA was most effective for triggering IL-1β-mediated cell death. Importantly, SMC-resistant cells that produced TNFα in response to IL-1β treatment were converted to an SMC-sensitive phenotype by c-FLIP knockdown. Reciprocally, ectopic expression of c-FLIP blocked cell death caused by combined SMC and IL-1β treatment in sensitive cancer cells. Together, our study indicates that a positive feed-forward loop by pro-inflammatory cytokines can be exploited by SMCs to induce apoptosis in cancer cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.