Four proteins governing overangiogenic endothelial cell phenotype in patients with multiple myeloma are plausible therapeutic targets.

摘要: Bone marrow (BM) angiogenesis has an important role in the initiation and progression of multiple myeloma (MM). We looked at novel mechanisms vessel formation patients with MM through a comparative proteomic analysis between BM endothelial cells (ECs) active (MMECs) ECs monoclonal gammopathy undetermined significance (MGECs) subjects benign anemia (normal ECs). Four proteins were found overexpressed MMECs: filamin A, vimentin, α-crystallin B 14-3-3ζ/δ protein, not yet linked to overangiogenic phenotype. These gave typical distribution MMECs versus MGECs, plausibly according different functional state. Their expression was enhanced by vascular growth factor, fibroblast factor 2, hepatocyte plasma cell conditioned medium step enhancement MMEC angiogenesis. silencing RNA knockdown affected critical angiogenesis-related functions, such as spreading, migration tubular morphogenesis. A gradual stabilization protein observed, transition from normal MGECs that may be for angiogenic switch maintenance substantially impacted anti-MM drugs, bortezomib, lenalidomide panobinostat. Results suggest these four could new targets antiangiogenic management patients.