ArticleBiological research2024
Lactadherin immunoblockade in small extracellular vesicles inhibits sEV-mediated increase of pro-metastatic capacities.
Article in Biological research, 2024. 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, 9 citations in OpenAlex.
- Extracellular vesicles in breast cancer metastasis: functional insights and advances in single-EV analysis.Cancer metastasis reviews · 2026Review
- Nuclear translocation of phosphorylated YB-1 via small extracellular vesicles contributes to the malignant phenotype of triple negative breast cancer.bioRxiv : the preprint server for biology · 2026Article
- Engineered extracellular vesicles for combinatorial cancer therapy and imaging.Acta pharmaceutica Sinica. B · 2026Review
- Small extracellular vesicles as system-level regulators and predictive biomarkers in breast cancer progression and chemoresistance.Frontiers in pharmacology · 2026Review
- Capture and detection of extracellular vesicles derived from human breast cancer cells using a 3D self-assembled nanostructured SiOJournal of biological engineering · 2025Article
- Maraviroc/cisplatin combination inhibits gastric cancer tumoroid growth and improves mice survival.Biological research · 2025Article
- Secreted LGALS3BP facilitates distant metastasis of breast cancer.Breast cancer research : BCR · 2025Article
- Effect Analysis of Extracellular Vesicles in the Treatment of Bronchopulmonary Dysplasia via Different Drug Delivery and Administration Routes.International journal of nanomedicine · 2025Review
- Iron-Reduced Graphene Oxide Core-Shell Micromotors Designed for Magnetic Guidance and Photothermal Therapy under Second Near-Infrared Light.Pharmaceutics · 2024Article
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7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTumor-derived small extracellular vesicles (sEVs) can promote tumorigenic and metastatic capacities in less aggressive recipient cells mainly through the biomolecules in their cargo. However, despite recent advances, the specific molecules orchestrating these changes are not completely defined. Lactadherin is a secreted glycoprotein typically found in the milk fat globule membrane. Its overexpression has been associated with increased tumorigenesis and metastasis in breast cancer (BC) and other tumors. However, neither its presence in sEVs secreted by BC cells, nor its role in sEV-mediated intercellular communication have been described. The present study focused on the role of lactadherin-containing sEVs from metastatic MDA-MB-231 triple-negative BC (TNBC) cells (sEV-MDA231) in the promotion of pro-metastatic capacities in non-tumorigenic and non-metastatic recipient cells in vitro, as well as their pro-metastatic role in a murine model of peritoneal carcinomatosis.
resultsWe show that lactadherin is present in sEVs secreted by BC cells and it is higher in sEV-MDA231 compared with the other BC cell-secreted sEVs measured through ELISA. Incubation of non-metastatic recipient cells with sEV-MDA231 increases their migration and, to some extent, their tumoroid formation capacity but not their anchorage-independent growth. Remarkably, lactadherin blockade in sEV-MDA231 results in a significant decrease of those sEV-mediated changes in vitro. Similarly, intraperitoneally treatment of mice with MDA-MB-231 BC cells and sEV-MDA231 greatly increase the formation of malignant ascites and tumor micronodules, effects that were significantly inhibited when lactadherin was previously blocked in those sEV-MDA231.
conclusionsAs to our knowledge, our study provides the first evidence on the role of lactadherin in metastatic BC cell-secreted sEVs as promoter of: (i) metastatic capacities in less aggressive recipient cells, and ii) the formation of malignant ascites and metastatic tumor nodules. These results increase our understanding on the role of lactadherin in sEVs as promoter of metastatic capacities which can be used as a therapeutic option for BC and other malignancies.
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