ArticleOncoTargets and therapy2020
Downregulation of IRAK1 Prevents the Malignant Behavior of Hepatocellular Carcinoma Cells by Blocking Activation of the MAPKs/NLRP3/IL-1β Pathway.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- NLRC4 and NLRP3 in tissues as potential biomarkers for the diagnosis of non-small cell lung cancer in pulmonary tuberculosis.Frontiers in cellular and infection microbiology · 2026Article
- IRAK signaling in cancers: mechanisms, targeting, and clinical implications.Expert opinion on investigational drugs · 2025Review
- CircCCT2/miR-146a-5p/IRAK1 axis promotes the development of head and neck squamous cell carcinoma.BMC cancer · 2025Article
- Dual role of pyroptosis in liver diseases: mechanisms, implications, and therapeutic perspectives.Frontiers in cell and developmental biology · 2025Review
- Review
- Recent Advances in IRAK1: Pharmacological and Therapeutic Aspects.Molecules (Basel, Switzerland) · 2024Review
- Article
- Dual roles of inflammatory programmed cell death in cancer: insights into pyroptosis and necroptosis.Frontiers in pharmacology · 2024Review
- Constructing a prognostic model for hepatocellular carcinoma based on bioinformatics analysis of inflammation-related genes.Frontiers in medicine · 2024Article
- Multifunctional roles of inflammation and its causative factors in primary liver cancer: A literature review.World journal of hepatology · 2023Review
- NLRP3 and cancer: Pathogenesis and therapeutic opportunities.Pharmacology & therapeutics · 2023Review
- The role of pyroptosis in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- IRAK2 Downregulation in Triple-Negative Breast Cancer Cells Decreases Cellular Growth In Vitro and Delays Tumour Progression in Murine Models.International journal of molecular sciences · 2023Article
- The Role of the NLRP3 Inflammasome in HCC Carcinogenesis and Treatment: Harnessing Innate Immunity.Cancers · 2022Review
- IL-1 receptor-associated kinase 1 participates in the modulation of the NLRP3 inflammasome by tumor-associated macrophages in hepatocellular carcinoma.Journal of gastrointestinal oncology · 2022Article
- A Pan-Cancer Analysis of IRAK1 Expression and Their Association With Immunotherapy Response.Frontiers in molecular biosciences · 2022Article
- Overcoming Immunotherapy Resistance by Targeting the Tumor-Intrinsic NLRP3-HSP70 Signaling Axis.Cancers · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionInterleukin-1 receptor-associated kinase 1 (IRAK1) was shown to contribute to a variety of cancer-related processes. However, the function of IRAK1 in hepatocellular carcinoma (HCC) pathogenesis has not been investigated in detail.
methodsIRAK1 expression in HCC was examined by immunohistochemistry, qRT-PCR, and Western blot assays. In addition, Huh7 and Hep3B cells were transfected with IRAK1 siRNAs and/or a NOD-like receptor family pyrindomain containing 3 (NLRP3) plasmid. Western blot, EdU staining, and Transwell assays were performed to determine changes of apoptosis, proliferation, migration, and invasion in HCC cells. Moreover, changes in the expression of proteins involved in the MAPKs/NLRP3/IL-1β pathway were confirmed by Western blotting.
resultsIRAK1 was found to be highly upregulated in HCC tissues and cells. Knockdown of IRAK1 signaling prevented the proliferation, invasion, migration, epithelial-mesenchymal transition (EMT) of HCC cells. Mechanistically, we found that activation of the MAPKs/NLRP3/IL-1β pathway could be markedly suppressed by IRAK1 knockdown in HCC cells. Furthermore, our data showed that NLRP3 could partially reverse the reduced aggressive biological behaviors of HCC cells which were caused by RAK1 knockdown.
conclusionKnockdown of
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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.