Osteolytic bone lesions are a common feature of multiple myeloma (MM). Proteosome inhibitors are used clinically to treat MM and act by disrupting endoplasmic reticulum associated degradation (ERAD) of misfolded proteins. We hypothesise that normal bone formation requires a fully functional ERAD. That is, whilst ERAD inhibition can stimulate mesenchymal stem cell (MSC) differentiation, the composition and structure of the material created will differ from that of native bone. Here, we examine the effects of ERAD inhibitors on MSC using biochemical assays, gene expression and immunostaining techniques. We also aim to determine the effects of ERAD inhibitors on bone quality.
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