ArticleThe Journal of cell biology2024
TNF and IFNγ-induced cell death requires IRF1 and ELAVL1 to promote CASP8 expression.
Article in The Journal of cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Intratumoral T cell activation kills tumors regardless of T cell specificity.Nature immunology · 2026Article
- CDK6 inactivation counteracts CALR-mutant-induced MPN evolution and sensitizes MPN stem cells to interferon-α treatment.HemaSphere · 2026Article
- Article
- A viable kinase-inactive RIPK3 D143N mouse model reveals its scaffold function in driving TNF-induced inflammatory disorder.Cell death discovery · 2026Article
- Regulated cell death in organ transplantation: recent developments and mechanistic overview.Journal of molecular cell biology · 2026Review
- The landscape of regulated cell death: It's all downhill from here.Molecular cell · 2026Review
- Epigenetic regulation of PANoptosis: DNA methylation, histone modifications and non-coding RNAs.EXCLI journal · 2026Review
- A non-apoptotic caspase-8-meteorin pathway in hepatocytes promotes MASH fibrosis.Nature metabolism · 2025Article
- Integrated pan-cancer analysis of RNA binding protein HuR investigates its biomarker potential in prognosis, immunotherapy, and drug sensitivity.PLoS computational biology · 2025Article
- Natural killer cell membrane manipulation for augmented immune synapse and anticancer efficacy.Materials today. Bio · 2025Review
- PANoptosis in neurological disorders: mechanisms, implications, and therapeutic potential.Frontiers in immunology · 2025Review
- RNA-binding protein HuR inhibition induces multiple programmed cell death in breast and prostate cancer.Cell communication and signaling : CCS · 2024Article
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12 authors at 2 institutions in 1 country.
Funding
Abstract
TNFα and IFNγ (TNF/IFNγ) synergistically induce caspase-8 activation and cancer cell death. However, the mechanism of IFNγ in promoting TNF-initiated caspase-8 activation in cancer cells is poorly understood. Here, we found that in addition to CASP8, CYLD is transcriptionally upregulated by IFNγ-induced transcription factor IRF1. IRF1-mediated CASP8 and CYLD upregulation additively mediates TNF/IFNγ-induced cancer cell death. Clinically, the expression levels of TNF, IFNγ, CYLD, and CASP8 in melanoma tumors are increased in patients responsive to immune checkpoint blockade (ICB) therapy after anti-PD-1 treatment. Accordingly, our genetic screen revealed that ELAVL1 (HuR) is required for TNF/IFNγ-induced caspase-8 activation. Mechanistically, ELAVL1 binds CASP8 mRNA and extends its stability to sustain caspase-8 expression both in IFNγ-stimulated and in basal conditions. Consequently, ELAVL1 determines death receptors-initiated caspase-8-dependent cell death triggered from stimuli including TNF and TRAIL by regulating basal/stimulated caspase-8 levels. As caspase-8 is a master regulator in cell death and inflammation, these results provide valuable clues for tumor immunotherapy and inflammatory diseases.
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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.