ArticleCancer science2024
Cross-talk between gastric cancer and hepatic stellate cells promotes invadopodia formation during liver metastasis.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- The biomechanical signature of tumor invasion.Genes & diseases · 2026Review
- Review
- A retrospective multicenter study on the efficacy and safety of disitamab vedotin monotherapy versus combination with anti-PD-1 immunotherapy in advanced gastric cancer.Scientific reports · 2025Article
- Review
- Molecular Mechanism for Malignant Progression of Gastric Cancer Within the Tumor Microenvironment.International journal of molecular sciences · 2024Review
- Cross-talk between gastric cancer and hepatic stellate cells promotes invadopodia formation during liver metastasis.Cancer science · 2024Article
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
In gastric cancer (GC), the liver is a common organ for distant metastasis, and patients with gastric cancer with liver metastasis (GCLM) generally have poor prognosis. The mechanism of GCLM is unclear. Invadopodia are special membrane protrusions formed by tumor cells that can degrade the basement membrane and ECM. Herein, we investigated the role of invadopodia in GCLM. We found that the levels of invadopodia-associated proteins were significantly higher in liver metastasis than in the primary tumors of patients with GCLM. Furthermore, GC cells could activate hepatic stellate cells (HSCs) within the tumor microenvironment of liver metastases through the secretion of platelet-derived growth factor subunit B (PDGFB). Activated HSCs secreted hepatocyte growth factor (HGF), which activated the MET proto-oncogene, MET receptor of GC cells, thereby promoting invadopodia formation through the PI3K/AKT pathway and subsequently enhancing the invasion and metastasis of GC cells. Therefore, cross-talk between GC cells and HSCs by PDGFB/platelet derived growth factor receptor beta (PDGFRβ) and the HGF/MET axis might represent potential therapeutic targets to treat GCLM.
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