ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2023
Soluble factors in malignant ascites promote the metastatic adhesion of gastric adenocarcinoma cells.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 5 citations in OpenAlex.
- Injectable multi-component hydrogels for the treatment of ascites caused by hepatocellular carcinoma via anti-tumor and reduction of ascites generation.Journal of nanobiotechnology · 2026Article
- Advances in protein microarray-based proteomics for gastric cancer applications in biomarker discovery, molecular subtyping, and precision oncology.Frontiers in oncology · 2026Review
- Emerging trends of the tumor microenvironment in peritoneal malignancies (2010-2024): a visualization analysis.Frontiers in oncology · 2025Article
- The role of microRNAs in the gastric cancer tumor microenvironment.Molecular cancer · 2024Review
- Malignant ascites supernatant enhances the proliferation of gastric cancer cells partially via the upregulation of asparagine synthetase.Oncology letters · 2023Article
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13 authors at 2 institutions in 1 country.
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Abstract
backgroundAdenocarcinoma of the proximal stomach is the fastest rising malignancy in North America. It is commonly associated with peritoneal accumulation of malignant ascites (MA), a fluid containing cancer and inflammatory cells and soluble proteins. Peritoneal metastasis (PM) is the most common site of gastric cancer (GC) progression after curative-intent surgery and is the leading cause of death among GC patients. METHODS/
resultsUsing a panel of gastric adenocarcinoma cell lines (human: MKN 45, SNU-5; murine: NCC-S1M), we demonstrate that prior incubation of GC cells with MA results in a significant (> 1.7-fold) increase in the number of cells capable of adhering to human peritoneal mesothelial cells (HPMC) (p < 0.05). We then corroborate these findings using an ex vivo PM model and show that MA also significantly enhances the ability of GC cells to adhere to strips of human peritoneum (p < 0.05). Using a multiplex ELISA, we identify MIF and VEGF as consistently elevated across MA samples from GC patients (p < 0.05). We demonstrate that agents that block the effects of MIF or VEGF abrogate the ability of MA to stimulate the adhesion of GC cells to adhere to human peritoneum and promote both ex vivo and in vivo metastases.
conclusionAgents targeting MIF or VEGF may be relevant to the treatment or prevention of PM in GC patients.
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