ArticleOncogene2021
Lymph node metastasis-derived gastric cancer cells educate bone marrow-derived mesenchymal stem cells via YAP signaling activation by exosomal Wnt5a.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 89 citations in OpenAlex.
- Small Extracellular Vesicle-TLN1 Modulates Gastric Cancer Cells and Remodels Lymphatic Endothelial Cells Through AKT Activation to Potentiate Lymphatic Metastasis.Cell biology international · 2026Article
- YAP1 Is a Crucial Nexus in the Tumor Microenvironment.Current medical science · 2026Review
- Exosome-orchestrated network in gastric cancer: mechanisms, immune regulation, biomarkers and therapeutic vehicles.Frontiers in cell and developmental biology · 2026Review
- The Spatiotemporal Heterogeneity of Tumor-Associated Stromal Cells: Reprogramming Plasticity to Unlock Precision Cancer Immunotherapy.Cancer communications (London, England) · 2026Review
- Remimazolam impairs bone marrow mesenchymal stem cell function and attenuates the tumor-promoting ability.American journal of translational research · 2026Article
- Exosome-mediated metabolic-immune regulatory axis: mechanisms of gastric cancer progression and resistance and targeting strategies.Frontiers in immunology · 2026Review
- KHDRBS3-mediated upregulation of circ_0024107 in gastric cancer cells and GC-MSCs synergistically drives gastric cancer cell migration and invasion.In vitro cellular & developmental biology. Animal · 2025Article
- WNT5a export onto extracellular vesicles studied at single-molecule and single-vesicle resolution.The FEBS journal · 2025Article
- Tumor-associated mesenchymal stem/stromal cells in tumor microenvironment and carcinogenesis.Experimental hematology & oncology · 2025Review
- Extracellular vesicles in cancer´s communication: messages we can read and how to answer.Molecular cancer · 2025Review
- Exosomes and their cargo proteins in diagnosis, process and treatment of gastric cancer.Frontiers in cell and developmental biology · 2025Review
- Extracellular vesicles: messengers of cross-talk between gastric cancer cells and the tumor microenvironment.Frontiers in cell and developmental biology · 2025Review
- Exosomal miR-224-3p promotes lymphangiogenesis and lymph node metastasis by targeting GSK3B in gastric cancer.Oncology research · 2025Article
- Exosome-derived proteins in gastric cancer progression, drug resistance, and immune response.Cellular & molecular biology letters · 2024Review
- The role of mesenchymal cells in cholangiocarcinoma.Disease models & mechanisms · 2024Article
- The Hippo signalling pathway in bone homeostasis: Under the regulation of mechanics and aging.Cell proliferation · 2024Review
- Unveiling heterogeneity in MSCs: exploring marker-based strategies for defining MSC subpopulations.Journal of translational medicine · 2024Review
- Cancer-derived exosomes as novel biomarkers in metastatic gastrointestinal cancer.Molecular cancer · 2024Review
- WNT Signaling in Stem Cells: A Look into the Non-Canonical Pathway.Stem cell reviews and reports · 2024Review
- The microprotein encoded by exosomal lncAKR1C2 promotes gastric cancer lymph node metastasis by regulating fatty acid metabolism.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymph node metastasis (LNM), a common metastatic gastric-cancer (GC) route, is closely related to poor prognosis in GC patients. Bone marrow-derived mesenchymal stem cells (BM-MSCs) preferentially engraft at metastatic lesions. Whether BM-MSCs are specifically reprogrammed by LNM-derived GC cells (LNM-GCs) and incorporated into metastatic LN microenvironment to prompt GC malignant progression remains unknown. Herein, we found that LNM-GCs specifically educated BM-MSCs via secretory exosomes. Exosomal Wnt5a was identified as key protein mediating LNM-GCs education of BM-MSCs, which was verified by analysis of serum exosomes collected from GC patients with LNM. Wnt5a-enriched exosomes induced YAP dephosphorylation in BM-MSCs, whereas Wnt5a-deficient exosomes exerted the opposite effect. Inhibition of YAP signaling by verteporfin blocked LNM-GC exosome- and serum exosome-mediated reprogramming in BM-MSCs. Analysis of MSC-like cells obtained from metastatic LN tissues of GC patients (GLN-MSCs) confirmed that BM-MSCs incorporated into metastatic LN microenvironment, and that YAP activation participated in maintaining their tumor-promoting phenotype and function. Collectively, our results show that LNM-GCs specifically educated BM-MSCs via exosomal Wnt5a-elicited activation of YAP signaling. This study provides new insights into the mechanisms of LNM in GC and BM-MSC reprogramming, and will provide potential therapeutic targets and detection indicators for GC patients with LNM.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.