ArticlePloS one2020
Cancer cell-derived interleukin-33 decoy receptor sST2 enhances orthotopic tumor growth in a murine pancreatic cancer model.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Diagnostic Value of Serum sST2 and MicroRNA-29a in Ovarian Cancer: A Dual-Biomarker Pilot Study.Current issues in molecular biology · 2026Article
- Downregulation of sST2, a decoy receptor for interleukin-33, enhances subcutaneous tumor growth in murine pancreatic cancer cells.FEBS open bio · 2025Article
- Integrating multi-omics data to identify the role of Aggrephagy-related genes in tumor microenvironment and key tumorigenesis factors of GB from the perspective of single-cell sequencing.Discover oncology · 2025Article
- Hypoxia induces downregulation of the tumor-suppressive sST2 in colorectal cancer cells via the HIF-nuclear IL-33-GATA3 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The role of IL-33/ST2 signaling in the tumor microenvironment and Treg immunotherapy.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- IL-33 induces ADAMTS5 expression and cell migration in glioblastoma multiforme.Medical oncology (Northwood, London, England) · 2022Article
- Inhibitory effect of lingonberry extract on HepG2 cell proliferation, apoptosis, migration, and invasion.PloS one · 2022Article
- Interference of LPSCells · 2021Article
- The role of alternative splicing in human cancer progression.American journal of cancer research · 2021Review
- Article
- Clinicopathological and Prognostic Relevance of Tumoral Suppression of Tumorigenicity 2 Expression in Patients With Surgically Resected Pancreatic Carcinoma.Cancer diagnosis & prognosisArticle
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundProinflammatory interleukin-33 (IL-33) binds to its receptor ST2L and is involved in inflammation and the malignant behavior of cancer cells. However, the role of IL-33-ST2L and the IL-33 decoy receptor sST2 in the tumor microenvironment of pancreatic cancer is unclear. Because we previously reported that sST2 derived from colon cancer cells profoundly influences malignant tumor growth, we hypothesized that sST2 released from pancreatic cancer cells also modulates IL-33-ST2L signaling in the tumor microenvironment, thereby influencing tumor growth.
methodsST2 (ST2L and sST2) expression in mouse pancreatic cancer Panc02 cells was downregulated by shRNAs. mRNA expression levels of IL-33, ST2, cytokines and chemokines in the cells and tumor tissues were examined using real-time PCR. sST2 secretion and the amount of CXCL3 in tumor tissues were measured using ELISA. Tumor growth was investigated after injection of the cells into the pancreas of C57BL/6 mice. MPO+, F4/80+ and CD20+ cells in tumor tissues were detected using immunohistochemistry.
resultsSome but not all human and mouse pancreatic cancer cell lines preferentially expressed sST2. Then, we investigated the role of sST2 in orthotopic tumor growth of sST2-expressing mouse pancreatic cancer Panc02 cells in immunocompetent mice. shRNA-mediated knockdown of sST2 expression in the cells suppressed orthotopic tumor growth, which was partially recovered by overexpression of shRNA-resistant sST2 mRNA but was not evident in IL-33 knockout mice. This was associated with decreases in Cxcl3 expression, vessel density and accumulation of cancer-associated neutrophils but not cancer-associated macrophages. Administration of SB225002, an inhibitor of the CXCL3 receptor CXCR2, induced similar effects.
conclusionsCancer cell-derived sST2 enhances tumor growth through upregulation of CXCL3 via inhibition of IL-33-ST2L signaling in the tumor microenvironment of pancreatic cancer. These results suggest that the sST2 and the CXCL3-CXCR2 axis could be therapeutic targets.
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