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Typically, secondary tumor formation within the bone microenvironment is considered a function of bone resorption because the degrading bone mineral matrix releases bioactive ions and growth factors critical to the proliferation of both normal and transformed cells [4], [11], [36], [37].
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The hypoxic microenvironment was considered to be one of the major factors contributing to GPI overexpression.
The bone microenvironment is also hypoxic [19].
Moreover, the bone microenvironment is known to support tumor growth in leukemia, myeloma and solid tumor bone metastasis [10], [11], [12], [13].
The preferential proliferation of cancer cells in the bone microenvironment is poorly characterised.
It is now generally accepted that the bone microenvironment is critical to the colonization and growth or dormancy of metastases.
Indeed, the bone microenvironment is characterized for the simultaneous presence of proinflammatory and anti-inflammatory mediators and cells.
Hierarchical structure mimicking the natural bone microenvironment has been considered as a promising platform to regulate cell functions.
It is also unknown whether ligands in the bone microenvironment are subjected to change in different physiological conditions.
The ability of HA to affect breast cancer cell colonization and tumor growth within the bone microenvironment was next assessed.
Recently, other cells of the bone microenvironment are emerging as implicated in bone health.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com