Abstract
Bone is the most common site of cancer metastasis and the spread of cancer cells to the bone is associated with poor prognosis, pain, increased risk of fractures, and hypercalcemia. The bone marrow microenvironment is an attractive place for tumor dissemination, due to the dynamic network of non-malignant cells. In particular, the alteration of the bone homeostasis favors the tumor homing and the consequent osteolytic or osteoblastic lesions. Extracellular vesicles (EVs) are reported to be involved in the metastatic process, promoting tumor invasion, escape from immune surveillance, extravasation, extracellular matrix remodeling, and metastasis, but the role of EVs in bone metastases is still unclear. Current results suggest the ability of tumor derived EVs in promoting bone localization and metastasis formation, altering the physiological balance between bone destruction and new bone depositions. Moreover, EVs from the bone marrow niche may support the onset of tumor metastasis. This review summarizes recent findings on the role of EVs in the pathological alterations of homeostasis that occur during bone metastasis to show novel potential EV-based therapeutic options to inhibit metastasis formation.
Highlights
Extracellular Vesicles: Biogenesis and CharacteristicsExtracellular vesicles (EVs) are lipidic membrane-delimited nanoparticles released by all cell types
Exosomes are derived from the invagination of the multivesicular bodies (MVBs) membrane and the formation of Extracellular Vesicles Enhance Bone Metastasis intraluminal vesicles (ILVs) [3, 4]
Mature MVBs can be directed to the degradation in lysosomes or fuse with the plasma membrane to release ILVs in the extracellular space as exosomes [4]
Summary
Extracellular vesicles (EVs) are lipidic membrane-delimited nanoparticles released by all cell types They are involved in physiologic and pathologic cellular communication. EVs represent a heterogeneous group of particles defined by size, shape, density, internal cargo, surface molecules, membrane components, cellular origin, and function [1] According to their biogenesis and size, EVs are classified in exosomes (30–100 nm); microvesicles (MVs) (100–1000 nm), and apoptotic bodies (> 2000 nm) [1, 2]. MVs are generated through the budding of the plasma membrane and their consequent release in the extracellular compartment [2] This event involves the redistribution of membrane proteins and lipids leading to changes in membrane stiffness and the final transfer of the molecular cargo in the MV lumen [9]. EVs exploit these mechanisms to transfer molecular messengers such as proteins, metabolites, lipids, mRNAs, and microRNAs (miRNAs) to target cells [12], affecting the functions and phenotypes of recipient cells by altering gene expression or by activating various signaling pathways [2]
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