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Published on: June 16, 2018
CD36-triggered cell invasion and persistent tissue colonization by tumor microvesicles during metastasis
Susanne Pfeiler1, Manovriti Thakur1, Petra Grünauer1
1Institut für Laboratoriumsmedizin, Klinikum der Universität München, Ludwig Maximilians Universität, Munich, Germany.
Tumor microvesicles use the CD36 receptor to interact with immune cells, facilitating their spread and colonization in the liver during metastasis. This CD36-dependent process involves microvesicle extravasation and persistent infiltration of tissue macrophages, promoting cancer metastasis.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- Tumor microvesicles are extracellular vesicles found in metastatic cancer patients' blood.
- Their role in immune cell interactions and metastasis progression is not fully understood.
Purpose of the Study:
- To investigate the role of the lipid receptor CD36 in tumor microvesicle trafficking and immune cell interactions during metastasis.
- To elucidate the mechanisms of tumor microvesicle engulfment, cargo delivery, and extravasation.
Main Methods:
- In vitro and in vivo studies using pancreatic tumor models in mice.
- Utilized nanoscopic imaging to observe individual tumor microvesicles.
- Investigated CD36-mediated engulfment by myeloid immune cells and liver macrophages.
Main Results:
- CD36 mediates the engulfment of tumor microvesicles by myeloid cells and is crucial for their uptake by liver macrophages.
- Tumor microvesicles rapidly decay upon engulfment, delivering cargo to the cytoplasm and plasma membrane.
- CD36 promotes tumor microvesicle extravasation and their colonization by perivascular macrophages, enhancing liver metastasis.
Conclusions:
- CD36 plays a critical role in regulating tumor microvesicle-immune cell interactions, promoting metastasis.
- CD36-dependent extravasation and macrophage colonization by tumor microvesicles contribute to pre-metastatic niche formation and liver metastasis development.
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