ArticleJournal of leukocyte biology2008
S100A8/A9 at low concentration promotes tumor cell growth via RAGE ligation and MAP kinase-dependent pathway.
Article in Journal of leukocyte biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
157 citing papers in PubMed, 2 syntheses or guidelines pooled it, 309 citations in OpenAlex.
- Calprotectin (S100A8/S100A9): a key protein between inflammation and cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Pooled it
- Pooled it
- Trial
- A Nutrient-Sensitive ZRF1-Dependent Secretory Network Involving S100A9 Contributes to Neutrophil Plasticity in Triple-Negative Breast Cancer.ACS pharmacology & translational science · 2026Article
- S100 signaling in hair follicle biology: emerging mechanistic insights and therapeutic opportunities.Journal of molecular histology · 2026Review
- Review
- S100A8/A9 inhibition reduces splenic myelopoiesis and improves outcomes after stroke.Frontiers in immunology · 2026Article
- Mass Spectrometry-Based Proteomics Analysis of Breast Milk for Breast Cancer Biomarker Discovery: An Update.Advances in experimental medicine and biology · 2026Review
- Emerging Biomarkers in Urological Cancers: Angiogenesis and Damage-Associated Molecular Pattern Signaling.International journal of molecular sciences · 2025Review
- Dynamics of Th1/Th17 responses and antimicrobial pathways in leprosy skin lesions.The Journal of clinical investigation · 2025Article
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- Shared Mechanisms in Cancer and Cardiovascular Disease: S100A8/9 and the NLRP3 Inflammasome: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2025Review
- The alarmin tandem: unraveling the complex effect of S100A8/A9 - from atherosclerosis to cardiac arrhythmias.Frontiers in immunology · 2025Review
- Single-cell RNA sequencing reveals that myeloid S100A8/A9 is a novel regulator of the transition from adaptive hypertrophy to heart failure after pressure overload.Theranostics · 2025Article
- Research progress on the diagnostic value of fecal calprotectin in colorectal tumors.Frontiers in medicine · 2025Review
- S100A8/A9 high-expression macrophages mediate renal tubular epithelial cell damage in acute kidney injury following acute type A aortic dissection surgery.Frontiers in molecular biosciences · 2025Article
- Microarray analysis of gene expression in lung tissues of indium-exposed rats: possible roles of S100 proteins in lung diseases.Archives of toxicology · 2025Article
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Persistent Activation of the P2X7 Receptor Underlies Chronic Inflammation and Carcinogenic Changes in the Intestine.International journal of molecular sciences · 2024Review
- Review
97 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
9 authors at 5 institutions in 4 countries.
Funding
Abstract
The complex formed by two members of the S100 calcium-binding protein family, S100A8/A9, exerts apoptosis-inducing activity against various cells, especially tumor cells. Here, we present evidence that S100A8/A9 also has cell growth-promoting activity at low concentrations. Receptor of advanced glycation end product (RAGE) gene silencing and cotreatment with a RAGE-specific blocking antibody revealed that this activity was mediated via RAGE ligation. To investigate the signaling pathways, MAPK phosphorylation and NF-kappaB activation were characterized in S100A8/A9-treated cells. S100A8/A9 caused a significant increase in p38 MAPK and p44/42 kinase phosphorylation, and the status of stress-activated protein kinase/JNK phosphorylation remained unchanged. Treatment of cells with S100A8/A9 also enhanced NF-kappaB activation. RAGE small interfering RNA pretreatment abrogated the S100A8/A9-induced NF-kappaB activation. Our data indicate that S100A8/A9-promoted cell growth occurs through RAGE signaling and activation of NF-kappaB.
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What OpenQuestion holds
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.