Data from Bone Morphogenetic Protein 7 in the Development and Treatment of Bone Metastases from Breast Cancer

• DOI: 10.1158/0008-5472.c.6495063.v1
• Publication Date: 2023-03-30T19:58:50Z
• Authors: Jeroen T. Buijs; Nico V. Henriquez; Petra G.M. van Ov...; Geertje van der H...; Ivo Que; Ruth Schwaninger; Cyrill Rentsch; Peter ten Dijke; Anne-Marie Cleton...; Keltouma Driouch; Rosette Lidereau; Richard Bachelier; Slobodan Vukicevic; Philippe Clézardin; Socrates E. Papap...; Marco G. Cecchini; Clemens W.G.M. Lo...; Gabri van der Pluijm

<div>Abstract<p>Bone morphogenetic protein 7 (BMP7) counteracts the physiological epithelial-to-mesenchymal transition (EMT), a process that is indicative of epithelial plasticity. Because EMT involved in cancer, we investigated whether BMP7 plays role breast cancer growth and metastasis. In this study, show decreased expression primary significantly associated with formation clinically overt bone metastases patients ≥10 years follow-up. line these clinical observations, inversely related to tumorigenicity invasive behavior human cell lines. Moreover, vimentin, mesenchymal marker invasiveness poor prognosis, MDA-MB-231 (MDA-231)-B/Luc<sup>+</sup> cells under basal transforming factor-β (TGF-β)–stimulated conditions. addition, exogenous addition TGF-β–stimulated MDA-231 inhibited Smad-mediated TGF-β signaling. Furthermore, well-established metastasis model using whole-body bioluminescent reporter imaging, stable overexpression <i>de novo</i> progression osteolytic and, hence, their metastatic capability. daily i.v. administration (100 μg/kg/d) orthotopic intrabone MDA-231-B/Luc<sup>+</sup> nude mice. Our data suggest during carcinogenesis contributes acquisition phenotype. can still counteract at site bone, may represent novel therapeutic molecule for repression local cancer. [Cancer Res 2007;67(18):8742–51]</p></div>