ArticleCellular oncology (Dordrecht, Netherlands)2022
IRAK2-NF-κB signaling promotes glycolysis-dependent tumor growth in pancreatic cancer.
Article in Cellular oncology (Dordrecht, Netherlands), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Research progress on the etiology and pathogenesis of pancreatic cancer: a narrative review.Frontiers in oncology · 2026Review
- KRAS-driven cytokine-metabolic crosstalk shapes immune exclusion in pancreatic ductal adenocarcinoma.Frontiers in genetics · 2026Review
- Article
- Shen Shuai II Recipe alleviates renal fibrosis in chronic kidney disease by improving of hypoxia and inhibition of TLR4/MyD88/NF-κB/NLRP3 pathway.Renal failure · 2025Article
- SUN5 interacts with TRIM28, enhancing IκBα ubiquitination to promote glycolysis in colorectal cancer cells.Acta biochimica et biophysica Sinica · 2025Article
- IRAK signaling in cancers: mechanisms, targeting, and clinical implications.Expert opinion on investigational drugs · 2025Review
- Global DNA methylomes reveal oncogenic-associated 5-hydroxylmethylated cytosine (5hmC) signatures in the cell-free DNA of cancer patients.medRxiv : the preprint server for health sciences · 2025Article
- TMEM105 modulates disulfidptosis and tumor growth in pancreatic cancer via the β-catenin-c-MYC-GLUT1 axis.International journal of biological sciences · 2025Article
- Spatial transcriptomic analysis of primary and metastatic pancreatic cancers highlights tumor microenvironmental heterogeneity.Nature genetics · 2024Article
- GJB2 Promotes HCC Progression by Activating Glycolysis Through Cytoplasmic Translocation and Generating a Suppressive Tumor Microenvironment Based on Single Cell RNA Sequencing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Versatile function of NF-ĸB in inflammation and cancer.Experimental hematology & oncology · 2024Review
- Gene Amplification of Mediator Subunit 30 Redirects the MYC Transcriptional Program and Oncogenesis.Research square · 2024Article
- Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis.International journal of molecular sciences · 2023Review
- IRAK2, an Immune and Radiation-Response Gene, Correlates with Advanced Disease Features but Predicts Higher Post-Irradiation Local Control in Non-Metastatic and Resected Oral Cancer Patients.International journal of molecular sciences · 2023Article
- Fucoxanthin suppresses the malignant progression of ovarian cancer by inactivating STAT3/c-Myc signaling.American journal of translational research · 2023Article
- WDR79 promotes aerobic glycolysis of pancreatic ductal adenocarcinoma (PDAC) by the suppression of SIRT4.Open medicine (Warsaw, Poland) · 2023Article
- Analyzing the impact of metabolism on immune cells in tumor microenvironment to promote the development of immunotherapy.Frontiers in immunology · 2023Review
- The significance of glycolysis in tumor progression and its relationship with the tumor microenvironment.Frontiers in pharmacology · 2022Review
- Glucose metabolism and tumour microenvironment in pancreatic cancer: A key link in cancer progression.Frontiers in immunology · 2022Review
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMetabolic reprogramming has emerged as a core hallmark of cancer, and cancer metabolism has long been equated with aerobic glycolysis. Moreover, hypoxia and the hypovascular tumor microenvironment (TME) are major hallmarks of pancreatic ductal adenocarcinoma (PDAC), in which glycolysis is imperative for tumor cell survival and proliferation. Here, we explored the impact of interleukin 1 receptor-associated kinase 2 (IRAK2) on the biological behavior of PDAC and investigated the underlying mechanism.
methodsThe expression pattern and clinical relevance of IRAK2 was determined in GEO, TCGA and Ren Ji datasets. Loss-of-function and gain-of-function studies were employed to investigate the cellular functions of IRAK2 in vitro and in vivo. Gene set enrichment analysis, Seahorse metabolic analysis, immunohistochemistry and Western blot were applied to reveal the underlying molecular mechanisms.
resultsWe found that IRAK2 is highly expressed in PDAC patient samples and is related to a poor prognosis. IRAK2 knockdown led to a significant impairment of PDAC cell proliferation via an aberrant Warburg effect. Opposite results were obtained after exogenous IRAK2 overexpression. Mechanistically, we found that IRAK2 is critical for sustaining the activation of transcription factors such as those of the nuclear factor-κB (NF-κB) family, which have increasingly been recognized as crucial players in many steps of cancer initiation and progression. Treatment with maslinic acid (MA), a NF-κB inhibitor, markedly attenuated the aberrant oncological behavior of PDAC cells caused by IRAK2 overexpression.
conclusionsOur data reveal a role of IRAK2 in PDAC metabolic reprogramming. In addition, we obtained novel insights into how immune-related pathways affect PDAC progression and suggest that targeting IRAK2 may serve as a novel therapeutic approach for PDAC.
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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.