ArticleCancer immunology, immunotherapy : CII2022
The role of S100A9 in the interaction between pancreatic ductal adenocarcinoma cells and stromal cells.
Article in Cancer immunology, immunotherapy : CII, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Proteomic Profiling of Extracellular Vesicle-Enriched Plasma Using Mag-Net for Biomarker Discovery in Pancreatic Ductal Adenocarcinoma.Journal of proteome research · 2026Article
- A Transgenic Mouse Model to Track MRC1-High Macrophages Using In Vivo Optical Imaging.International journal of molecular sciences · 2026Article
- Role of S100 family proteins in colorectal cancer (CRC): an overview of their potential function as new biomarkers and therapeutic agents.Expert reviews in molecular medicine · 2025Review
- PGAM5 interacts with and maintains BNIP3 to license cancer-associated muscle wasting.Autophagy · 2024Article
- CD74 Promotes a Pro-Inflammatory Tumor Microenvironment by Inducing S100A8 and S100A9 Secretion in Pancreatic Cancer.International journal of molecular sciences · 2023Article
- S100A8, S100A9 and S100A8/A9 heterodimer as novel cachexigenic factors for pancreatic cancer-induced cachexia.BMC cancer · 2023Article
- Characterization of 3D heterocellular spheroids of pancreatic ductal adenocarcinoma for the study of cell interactions in the tumor immune microenvironment.Frontiers in oncology · 2023Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
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Abstract
backgroundA major feature of the microenvironment in pancreatic ductal adenocarcinoma (PDAC) is the significant amount of extracellular matrix produced by pancreatic stellate cells (PSCs), which have been reported to enhance the invasiveness of pancreatic cancer cells and negatively impact the prognosis.
methodsWe analyzed the data from two publicly available microarray datasets deposited in the Gene Expression Omnibus and found candidate genes that were differentially expressed in PDAC cells with metastatic potential and PDAC cells cocultured with PSCs. We studied the interaction between PDAC cells and PSCs in vitro and verified our finding with the survival data of patients with PDAC from the website of The Human Protein Atlas.
resultsWe found that PSCs stimulated PDAC cells to secrete S100A9, which attracted circulatory monocytes into cancer tissue and enhanced the expression of programmed death-ligand 1 (PD-L1) on macrophages. When analyzing the correlation of S100A9 and PD-L1 expression with the clinical outcomes of patients with PDAC, we ascertained that high expression of S100A9 and PD-L1 was associated with poor survival in patients with PDAC.
conclusionsPSCs stimulated PDAC cells to secrete S100A9, which acts as a chemoattractant to attract circulatory monocytes into cancer microenvironment and induces expression of PD-L1 on macrophages. High expression of S100A9 and PD-L1 was associated with worse overall survival in a cohort of patients with PDAC.
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