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hrCCN5 (human recombinant CCN5) is a recombinant form of the human matricellular protein CCN5 (also known as WNT1-inducible-signaling pathway protein 2, or WISP-2). CCN5 is a unique member of the CCN family that lacks the C-terminal (CT) domain, which typically mediates pro-fibrotic and pro-angiogenic activities in other family members. Developed primarily by researchers at the Kansas City VA Medical Center and the University of Kansas Medical Center, hrCCN5 is being investigated as a therapeutic agent for triple-negative breast cancer (TNBC) and cardiac fibrosis. In TNBC, hrCCN5 acts as a tumor suppressor by reversing epithelial-to-mesenchymal transition (EMT), inhibiting cell proliferation, and restoring estrogen receptor-alpha (ERα) expression, thereby sensitizing TNBC cells to endocrine therapies like tamoxifen. In cardiac models, hrCCN5 inhibits and reverses the trans-differentiation of cardiac fibroblasts into myofibroblasts, offering a potential treatment for cardiac fibrosis and heart failure.
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