ArticleFEBS open bio2025
Downregulation of sST2, a decoy receptor for interleukin-33, enhances subcutaneous tumor growth in murine pancreatic cancer cells.
Article in FEBS open bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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.
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Who cites it
1 citing paper in PubMed.
- Diagnostic Value of Serum sST2 and MicroRNA-29a in Ovarian Cancer: A Dual-Biomarker Pilot Study.Current issues in molecular biology · 2026Article
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Authors and funding
6 authors.
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Abstract
Despite the recent scientific advancements, pancreatic cancer remains the seventh leading cause of cancer-related mortality. Pancreatic cancer progression is closely associated with inflammation, and we previously showed that short hairpin RNA-mediated knockdown of sST2 expression, a soluble decoy receptor for the proinflammatory molecule interleukin-33 (IL-33), in mouse Panc02 pancreatic cancer cells reduced malignant growth following pancreatic (orthotopic) implantation. Furthermore, this growth suppression was accompanied by decreased tumor angiogenesis, reduced expression of the neutrophil chemoattractant CXCL3, and a lower number of tumor-associated neutrophils (TANs). In contrast to previous results, in this study, we showed that IL-33-dependent tumor growth and pulmonary metastasis occurred following subcutaneous (ectopic) implantation of sST2-knockdown cells. This was associated with a decrease in the levels of the anti-inflammatory molecule adiponectin and the number of GLUT4-positive cancer-associated adipocytes, as well as an increase in IκBα phosphorylation levels, Cxcl3 expression, and the accumulation of infiltrating CD206
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