Therapies targeting bone-degrading cells are the current standard of care for combating cancer metastasis in the skeleton. These cells are directed by cancer cells to degrade bone in order to release pro-tumorigenic growth factors stored within the skeletal extracellular matrix. These therapies are not curative and do not halt metastasis-mediated bone degradation, indicating additional factors contribute to bone degradation. My research program focuses on the skeletal mechanical environment and its role in cancer regulation. Specifically, I investigate 1) mechanoregulation of bone metastatic cancer cells, and 2) the role of bone-forming osteoblastic cells, which comprise the principal sensor and effector cells of mechanical cues, in metastatic processes. My experimental approach uses novel in vivo and in vitro mechanical loading model systems to correlate cellular function with tissue-level changes in tumor burden and skeletal tissue strength.
biomechanics, mechanobiology, cancer, bone, mechanical loading, 3D models