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- W2805299898 abstract "Abstract Semaphorin 3A (Sema3A), a secreted member of the Semaphorin family, increases osteoblast differentiation, stimulates bone formation and enhances fracture healing. Here, we report a previously unknown role of Sema3A in the regulation of ectopic bone formation and osteolysis related to osteosarcoma. Human recombinant (exogenous) Sema3A promoted the expression of osteoblastic phenotype in a panel of human osteosarcoma cell lines and inhibited the ability of these cells to migrate and enhance osteoclastogenesis in vitro . In vivo , administration of exogenous Sema3A in mice after paratibial inoculation of KHOS cells increased bone volume in non-inoculated and tumour-bearing legs. In contrast, Sema3A overexpression reduced the ability of KHOS cells to cause ectopic bone formation in mice and to increase bone nodule formation by engaging DKK1/β-catenin signalling. Thus, Sema3A is of potential therapeutic efficacy in osteosarcoma. However, inhibition of bone formation associated with continuous exposure to Sema3A may limit its long-term usefulness as therapeutic agent." @default.
- W2805299898 created "2018-06-13" @default.
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- W2805299898 date "2018-05-02" @default.
- W2805299898 modified "2023-10-02" @default.
- W2805299898 title "Bidirectional regulation of bone formation by exogenous and osteosarcoma-derived Sema3A" @default.
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- W2805299898 doi "https://doi.org/10.1038/s41598-018-25290-2" @default.
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