Abstract
The bone microenvironment homeostasis is guaranteed by the balanced and fine regulated bone matrix remodeling process. This equilibrium can be disrupted by cancer cells developed in the bone (primary bone cancers) or deriving from other tissues (bone metastatic lesions), through a mechanism by which they interfere with bone cells activities and alter the microenvironment both biochemically and mechanically. Among the factors secreted by cancer cells and by cancer-conditioned bone cells, extracellular vesicles (EVs) are described to exert pivotal roles in the establishment and the progression of bone cancers, by conveying tumorigenic signals targeting and transforming normal cells. Doing this, EVs are also responsible in modulating the production of proteins involved in regulating matrix stiffness and/or mechanotransduction process, thereby altering the bone mechanoenvironment. In turn, bone and cancer cells respond to deregulated matrix stiffness by modifying EV production and content, fueling the vicious cycle established in tumors. Here, we summarized the relationship between EVs and the mechanoenvironment during tumoral progression, with the final aim to provide some innovative perspectives in counteracting bone cancers.
Highlights
Bone primary tumors are a heterogeneous group of rare neoplasms of the skeleton, accounting for approximately 0.2% of all tumors (Franchi, 2012)
Here we summarized the mutual relationship between extracellular vesicles and the mechanoenvironment in the context of bone tumors, both primary and metastatic, with the final aim to provide some novel points of view to counteract cancer by considering the roles exerted by EVs and the tissue biomechanics
EVs released by cancer cells or by transformed bone cells are involved in altering the bone microenvironment and the bone matrix, thereby causing the deregulation of the stiffness and the mechanics properties of the tissue (Figure 1)
Summary
Bone primary tumors are a heterogeneous group of rare neoplasms of the skeleton, accounting for approximately 0.2% of all tumors (Franchi, 2012). To reduce osteoblast differentiation and type1 collagen deposition To impair osteolytic lesions and bone colonization by decreasing tumor-induced osteoclastogenesis and angiogenesis in vivo To favor the differentiation and the resorbing activity of osteoclasts, supporting the formation of a pre-metastatic niche
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