ArticleExperimental & molecular medicine2023
Caveolin-1 mediates the utilization of extracellular proteins for survival in refractory gastric cancer.
Article in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- RNF214 silencing attenuates prostate cancer progression and modulates mTOR signaling through CAV1 ubiquitination.Cell & bioscience · 2026Article
- A lipid-centric view of endocytosis by caveolae.Nature cell biology · 2026Review
- 1,3-and 1,4-linked polysaccharides uptake in intestinal cells relies on clathrin/dynamin 1/Rab5-dependent endocytosis.Nature communications · 2026Article
- Patient-derived organoids in gastric cancer: bridging the tumor microenvironment to functional precision oncology.Frontiers in bioengineering and biotechnology · 2026Review
- Analysis of the expression of FAP, Caveolin1, and CPXM2 and prognostic significance in gastric cancer.Frontiers in oncology · 2026Article
- Orchestrating movement: the role of Caveolin-1 in migration and metastasis.Molecular cancer · 2025Review
- One-carbon metabolic pathway is a novel molecular signature for CD44-positive intestinal-type gastric cancer.Cell death discovery · 2025Article
- Clinicopathological Significance and Prognostic Value of the Caveolae Constitutive Proteins Dynamin-2 and Caveolin-1 in Oral Squamous Cell Carcinoma.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2025Article
- PDGFR-β/Cav1-induced autophagy via mTOR/FIP200/ATG13 activation in cancer-associated fibroblasts promotes the malignant progression of breast cancer.Journal of translational medicine · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Despite advances in cancer therapy, the clinical outcome of patients with gastric cancer remains poor, largely due to tumor heterogeneity. Thus, finding a hidden vulnerability of clinically refractory subtypes of gastric cancer is crucial. Here, we report that chemoresistant gastric cancer cells rely heavily on endocytosis, facilitated by caveolin-1, for survival. caveolin-1 was highly upregulated in the most malignant stem-like/EMT/mesenchymal (SEM)-type gastric cancer cells, allowing caveolin-1-mediated endocytosis and utilization of extracellular proteins via lysosomal degradation. Downregulation of caveolin-1 alone was sufficient to induce cell death in SEM-type gastric cancer cells, emphasizing its importance as a survival mechanism. Consistently, chloroquine, a lysosomal inhibitor, successfully blocked caveolin-1-mediated endocytosis, leading to the marked suppression of tumor growth in chemorefractory gastric cancer cells in vitro, including patient-derived organoids, and in vivo. Together, our findings suggest that caveolin-1-mediated endocytosis is a key metabolic pathway for gastric cancer survival and a potential therapeutic target.
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