ArticleCellular and molecular gastroenterology and hepatology2025
Cortactin Facilitates Malignant Transformation of Dysplastic Cells in Gastric Cancer Development.
Article in Cellular and molecular gastroenterology and hepatology, 2025. 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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Who cites it
5 citing papers in PubMed.
- Review
- Rab27: Molecular switch of tumor exosome secretion (Review).International journal of molecular medicine · 2026Review
- Organoids in cancer therapy: translational applications and clinical promise.Molecular cancer · 2026Review
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- Exosome-orchestrated network in gastric cancer: mechanisms, immune regulation, biomarkers and therapeutic vehicles.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
9 authors.
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Abstract
BACKGROUND &
aimsEpithelial cancer onset occurs through sequential stages of cell lineage conversion and functional dysregulation. Dysplasia is a precancerous lesion defined as a direct precursor to cancer and is histologically defined as a transition stage between pre-cancer and cancer, but molecular and biological mechanisms controlling its transformation to malignancy are underdetermined. Here, we discover the crucial role of the actin stabilization and exosome secretion-regulatory protein cortactin in dysplastic cell transformation to adenocarcinoma.
methodsWe engineered a CRISPR/Cas9-based cortactin knock-out (KO) dysplasia organoid model established from dysplastic tissue and examined malignant roles of cortactin during gastric cancer development in vitro and in vivo.
resultsAlthough dysplastic cell identity remained unchanged, the cortactin KO organoids exhibited a decrease in cellular organization and multicellular protrusions, which are considered aggressive features when observed in vitro. When injected into the flank of nude mice, cortactin KO cells failed malignant transformation into adenocarcinoma and solid tumor formation with reduced recruitment of fibroblasts and macrophages. In addition, cortactin KO cells showed diminished exosome secretion levels, and adenocarcinoma development was impaired when exosome secretion was inhibited in cortactin wild-type dysplastic cells.
conclusionsThese data suggest that cortactin is a functional element of membrane dynamics, malignant changes, and exosome secretion in dysplastic cells, and solid gastric tumor formation associated with alteration of the tumor microenvironment.
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