Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET
Open accessAbstract
Tumor-derived exosomes are emerging mediators of tumorigenesis. We explored the function of melanoma-derived exosomes in the formation of primary tumors and metastases in mice and human subjects. Exosomes from highly metastatic melanomas increased the metastatic behavior of primary tumors by permanently 'educating' bone marrow progenitors through the receptor tyrosine kinase MET. Melanoma-derived exosomes also induced vascular leakiness at pre-metastatic sites and reprogrammed bone marrow progenitors toward a pro-vasculogenic phenotype that was positive for c-Kit, the receptor tyrosine kinase Tie2 and Met. Reducing Met expression in exosomes diminished the pro-metastatic behavior of bone marrow cells. Notably, MET expression was elevated in circulating CD45(-)C-KIT(low/+)TIE2(+) bone marrow progenitors from individuals with metastatic melanoma. RAB1A, RAB5B, RAB7 and RAB27A, regulators of membrane trafficking and exosome formation, were highly expressed in melanoma cells. Rab27A RNA interference decreased exosome production, preventing bone marrow education and reducing, tumor growth and metastasis. In addition, we identified an exosome-specific melanoma signature with prognostic and therapeutic potential comprised of TYRP2, VLA-4, HSP70, an HSP90 isoform and the MET oncoprotein. Our data show that exosome production, transfer and education of bone marrow cells supports tumor growth and metastasis, has prognostic value and offers promise for new therapeutic directions in the metastatic process.
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Tumor-derived exosomes preferentially localize to sites of metastasis including liver, lung, and bone marrow, where they promote vascular permeability and increase BMDC recruitment.
“Moreover, tumor-derived exosomes preferentially localize to sites of metastasis, including liver, lung, and bone marrow, where they promote vascular permeability and increase BMDC recruitment (101–104).”
From Hypoxic control of metastasis (2016) · cites this paper as [101]
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- Authors
- Peinado, H., Alečković, M., Lavotshkin, S., Matei, I., Costa-Silva, B., Moreno-Bueno, G., Hergueta-Redondo, M., Williams, C., García-Santos, G., Ghajar, C. M., Nitadori-Hoshino, A., Hoffman, C., Badal, K., Garcia, B. A., Callahan, M. K., Yuan, J., Martins, V. R., Skog, J., Kaplan, R. N., Brady, M. S., Wolchok, J. D., Chapman, P. B., Kang, Y., Bromberg, J., & Lyden, D.
- Affiliations
- Children's Cancer and Blood Foundation (US)
- Princeton University (US)
- Columbia University (US)
- Lawrence Berkeley National Laboratory (US)
- Weill Cornell Medicine (US)
- Memorial Sloan Kettering Cancer Center (US)
- AC Camargo Hospital (BR)
- Exosome Diagnostics (United States) (US)
- National Institutes of Health (US)
- Champalimaud Foundation (PT)
- Corresponding author
- Bromberg, Jacqueline
- Lyden, David
- ORCID
- Venue
- Nature Medicine
- Published
- 2012-05-27
- Volume
- 18
- Issue
- 6
- Pages
- 883-891
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3645291
- OpenAlex
- W2169491358
- Cited by
- 3,715
- References
- 3
- Citations by year
- 2026: 123 · 2025: 176 · 2024: 228 · 2023: 224 · 2022: 287 · 2021: 383 · 2020: 361 · 2019: 324 · 2018: 329 · 2017: 311 · 2016: 312 · 2015: 261 · 2014: 212 · 2013: 149 · 2012: 31
- FWCI
- 84.01
- Type
- journal article
- Language
- en
- Update notices
- erratum (2016-12-06)
- Open access
- green
- europepmc.org
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Funders
- National Cancer Institute (R01CA087637, R01CA098234, R01CA141062, U54CA143836, CA87637, R01CA134519)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- melanoma, tumor-derived exosomes, bone marrow progenitor cells, MET receptor tyrosine kinase, metastasis, CD117, Tie2, Rab27a, vascular leakage, prognostic signature, HSP90, HSP70, VLA-4, tyrosinase-related protein 2, exosome transfer
- MeSH terms
- rab27 GTP-Binding Proteins, Animals, Bone Marrow Cells, Cell Line, Female, Humans, Melanoma, Mice, Inbred C57BL, Phenotype, Prognosis, Stem Cells, Proto-Oncogene Proteins c-met, rab GTP-Binding Proteins, Mice, Exosomes
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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