Study shows that mineralization of bone matrix regulates tumor cell growth

An interdisciplinary Cornell team has identified a new mechanism regulating tumor growth in the skeleton, the primary site of breast cancer metastasis: mineralization of the bone matrix, a fibrous mesh of organic and inorganic components that determines the unique biochemical and biomechanical properties of our skeleton.

A connection between reduced bone health and the behavior of tumor cells is well-established. For example, decreased bone-mineral density has been correlated with increased risk for metastasis, and incomplete fracture healing has been shown to enhance bone metastasis. However, no one had been able to isolate which specific role bone-matrix mineralization plays in this process.

The researchers were able to create such systems by combining organic and inorganic matrix components, including collagen and the bone mineral hydroxyapatite, in a manner that mimicked physiological and pathologic mineralization.The necessary materials synthesis was carried out and characterization techniques of the different bone matrix models, which the team then used to investigate tumor cell behavior, first in vitro and then in vivo through mouse models.

The presence of bone mineral reduced the growth of tumor cells in both settings. The presence of mineral also caused tumor cells to promote genes that were associated with better patient prognosis. These findings suggest that healthy bone matrix can reduce the risk for breast cancer skeletal metastasis.

Reference: Nature Biomedical Engineering, DOI 10.1038/s41551-023-01077-3