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Updated: Jun 23, 2026
A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis
Published on: March 8, 2022
Tumor-derived microvesicles modulate the establishment of metastatic melanoma in a phosphatidylserine-dependent
Luize G Lima1, Roger Chammas, Robson Q Monteiro
1Division of Experimental Medicine, National Cancer Institute, RJ, Brazil; Institute of Medical Biochemistry, Federal University of Rio de Janeiro, RJ, Brazil. lglima@bioqmed.ufrj.br
Abstract:
Exposure of phosphatidylserine (PS) on cellular membranes and membrane-derived microvesicles stimulates a number of anti-inflammatory responses involved in malignant processes. Herein we show that B16F10 cells, a highly metastatic melanoma cell line, produce large quantities of PS-containing microvesicles in vitro. Tumor microvesicles increased TGF-beta(1) production by cultured macrophages and, in vivo, enhanced the metastatic potential of B16F10 cells in C57BL/6 mice, both effects being reversed by annexin V. Most strikingly, microvesicles induced melanoma metastasis in BALB/c mice, which are normally resistant to this tumor cell line. Altogether, this is the first demonstration that tumor-derived microvesicles favor the establishment of melanoma metastasis in a PS-dependent manner, possibly by down-regulating the host's inflammatory and/or anti-tumoral immune responses.
Insights
Tumor microvesicles containing phosphatidylserine (PS) promote melanoma metastasis by suppressing immune responses. Annexin V reversed these pro-metastatic effects, highlighting PS
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- Phosphatidylserine (PS) exposure on microvesicles influences inflammatory responses in malignancy.
- B16F10 melanoma cells generate abundant PS-containing microvesicles in vitro.
Purpose of the Study:
- To investigate the role of PS-containing tumor microvesicles in melanoma metastasis.
- To determine if these microvesicles can overcome host resistance to melanoma.
Main Methods:
- In vitro analysis of PS-microvesicle production by B16F10 cells.
- Assessment of microvesicle effects on macrophage TGF-beta(1) production.
- In vivo studies of B16F10 cell metastasis in C57BL/6 and BALB/c mice, with and without annexin V treatment.
Main Results:
- B16F10 microvesicles increased macrophage TGF-beta(1) production.
- Microvesicles enhanced B16F10 cell metastasis in C57BL/6 mice.
- Microvesicles induced metastasis in normally resistant BALB/c mice.
- Annexin V reversed the pro-metastatic effects of microvesicles.
Conclusions:
- Tumor-derived microvesicles promote melanoma metastasis in a PS-dependent manner.
- These microvesicles may facilitate metastasis by down-regulating host anti-tumoral immunity.
- This study provides the first evidence of microvesicles driving melanoma metastasis via PS signaling.
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