ArticleOncogene2015
Mutant p53 gains new function in promoting inflammatory signals by repression of the secreted interleukin-1 receptor antagonist.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- The pivotal role of macrophages in tumorigenesis and pioneering cancer immunotherapy across pre-clinical and clinical frontiers.Journal of cancer research and clinical oncology · 2026Review
- Outcomes of hemophagocytic lymphohistiocytosis in acute myeloid leukemia: the 3-site Mayo Clinic experience.Blood neoplasia · 2026Article
- Natural products as therapeutic interventions for inflammation-mediated cancer.Discover oncology · 2025Review
- Predictive factors for neoadjuvant combined immunotherapy in gastric adenocarcinoma: Focusing on the primitive enterocyte phenotype and PVR.British journal of cancer · 2025Article
- The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs.Biomolecules · 2025Review
- The fibroinflammatory response in cancer.Nature reviews. Cancer · 2025Review
- AAV vectors trigger DNA damage response-dependent pro-inflammatory signalling in human iPSC-derived CNS models and mouse brain.Nature communications · 2025Article
- Multifaceted Aspects of Dysfunctional Myelopoiesis in Cancer and Therapeutic Perspectives with Focus on HCC.Biomolecules · 2024Review
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- The Clinical and Molecular Profile of Lung Cancer Patients Harboring theInternational journal of molecular sciences · 2023Article
- UBE2T promotes glioblastoma malignancy through ubiquitination-mediated degradation of RPL6.Cancer science · 2023Article
- Mutant p53 in cancer: from molecular mechanism to therapeutic modulation.Cell death & disease · 2022Review
- Mutant p53 gain of function mediates cancer immune escape that is counteracted by APR-246.British journal of cancer · 2022Article
- Immune cellular components and signaling pathways in the tumor microenvironment.Seminars in cancer biology · 2022Review
- Review
- Long noncoding RNA H19 alleviates inflammation in osteoarthritis through interactions between TP53, IL-38, and IL-36 receptor.Bone & joint research · 2022Article
- The complex role of tumor-infiltrating macrophages.Nature immunology · 2022Review
- Amino acid sensor GCN2 promotes SARS-CoV-2 receptor ACE2 expression in response to amino acid deprivation.Communications biology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The TP53 tumor-suppressor gene is frequently mutated in human cancer. Missense mutations can add novel functions (gain-of-function, GOF) that promote tumor malignancy. Here we report that mutant (mut) p53 promotes tumor malignancy by suppressing the expression of a natural occurring anti-inflammatory cytokine, the secreted interleukin-1 receptor antagonist (sIL-1Ra, IL1RN). We show that mutp53 but not wild-type (wt) p53 suppresses the sIL-1Ra production in conditioned media of cancer cells. Moreover, mutp53, but not wtp53, binds physically the sIL-1Ra promoter and the protein-protein interaction with the transcriptional co-repressor MAFF (v-MAF musculoaponeurotic fibrosarcoma oncogene family, protein F) is required for mutp53-induced sIL-1Ra suppression. Remarkably, when exposed to IL-1 beta (IL-1β) inflammatory stimuli, mutp53 sustains a ready-to-be-activated in vitro and in vivo cancer cells' response through the sIL-1Ra repression. Taken together, these results identify sIL-1Ra as a novel mutp53 target gene, whose suppression might be required to generate a chronic pro-inflammatory tumor microenvironment through which mutp53 promotes tumor malignancy.
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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.