ArticleCancer research2009
The receptor interacting protein 1 inhibits p53 induction through NF-kappaB activation and confers a worse prognosis in glioblastoma.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 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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Who cites it
101 citing papers in PubMed, 153 citations in OpenAlex.
- Programmed cell death in cancer: targeting necroptosis to kill tumor cell.Cell death discovery · 2026Review
- Unlocking glioma vulnerabilities: targeting regulated cell death pathways for innovative therapies.Cell death discovery · 2026Review
- Targeting RIPK1 to modulate cell death and tumour microenvironment in cancer therapy.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Mechanism and role of regulated cell death in tumor immunity and immunotherapy.Cancer communications (London, England) · 2025Review
- Crosstalk between non-coding RNAs and programmed cell death in colorectal cancer: implications for targeted therapy.Epigenetics & chromatin · 2025Review
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- Proteomic Stratification of Prognosis and Treatment Options for Small Cell Lung Cancer.Genomics, proteomics & bioinformatics · 2024Article
- Non-apoptotic regulated cell death mediates reprogramming of the tumour immune microenvironment by macrophages.Journal of cellular and molecular medicine · 2024Review
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- Dual roles of inflammatory programmed cell death in cancer: insights into pyroptosis and necroptosis.Frontiers in pharmacology · 2024Review
- Identification and validation of a novel necroptosis-related molecular signature to evaluate prognosis and immune features in breast cancer.Apoptosis : an international journal on programmed cell death · 2023Article
- Roles of RIPK1 as a stress sentinel coordinating cell survival and immunogenic cell death.Nature reviews. Molecular cell biology · 2023Review
- Genetic variants in key necroptosis regulators predict prognosis of non-small cell lung cancer after surgical resection.Thoracic cancer · 2023Article
- The Dual Role of Necroptosis in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2023Review
- MiR-204-3p overexpression inhibits gastric carcinoma cell proliferation by inhibiting the MAPK pathway and RIP1/MLK1 necroptosis pathway to promote apoptosis.World journal of gastroenterology · 2023Article
- The roles of long non-coding RNAs in the necroptotic signaling of colon cancer cells.Molecular biology reports · 2023Article
- Construction and validation of a prognostic signature based on necroptosis-related genes in hepatocellular carcinoma.PloS one · 2023Article
- Development and validation of a novel necroptosis-related gene signature for predicting prognosis and therapeutic response in Ewing sarcoma.Frontiers in medicine · 2023Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 1 country.
Funding
Abstract
Nuclear factor-kappaB (NF-kappaB) activation may play an important role in the pathogenesis of cancer and also in resistance to treatment. Inactivation of the p53 tumor suppressor is a key component of the multistep evolution of most cancers. Links between the NF-kappaB and p53 pathways are under intense investigation. In this study, we show that the receptor interacting protein 1 (RIP1), a central component of the NF-kappaB signaling network, negatively regulates p53 tumor suppressor signaling. Loss of RIP1 from cells results in augmented induction of p53 in response to DNA damage, whereas increased RIP1 level leads to a complete shutdown of DNA damage-induced p53 induction by enhancing levels of cellular mdm2. The key signal generated by RIP1 to up-regulate mdm2 and inhibit p53 is activation of NF-kappaB. The clinical implication of this finding is shown in glioblastoma, the most common primary malignant brain tumor in adults. We show that RIP1 is commonly overexpressed in glioblastoma, but not in grades II and III glioma, and increased expression of RIP1 confers a worse prognosis in glioblastoma. Importantly, RIP1 levels correlate strongly with mdm2 levels in glioblastoma. Our results show a key interaction between the NF-kappaB and p53 pathways that may have implications for the targeted treatment of glioblastoma.
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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.