Abstract:
:The osteolytic bone destruction associated with breast cancer skeletal metastases represents a serious and incurable clinical condition. However, the molecular mechanisms regulating tumor cell expression of factors involved in the generation of osteolytic disease remain elusive. We demonstrated recently that breast cancer cells express the Runx2 transcription factor, essential for bone formation and a regulator of skeletal homeostasis. Our experimental results demonstrate that perturbation of Runx2 regulatory function in tumor cells abolishes their ability to form osteolytic lesions in vivo. In vitro, we show that breast cancer cells inhibit osteoblast differentiation while concurrently enhancing osteoclast differentiation in marrow stromal cell cultures. Disruption of Runx2 activity abrogates both of these cancer cell-mediated effects on bone cells. These results demonstrate that Runx2 expression in breast cancer cells provides a molecular phenotype that enables the interactions between tumor cells and the bone microenvironment that lead to osteolytic disease.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Barnes GL,Hebert KE,Kamal M,Javed A,Einhorn TA,Lian JB,Stein GS,Gerstenfeld LCdoi
10.1158/0008-5472.CAN-03-3851subject
Has Abstractpub_date
2004-07-01 00:00:00pages
4506-13issue
13eissn
0008-5472issn
1538-7445pii
64/13/4506journal_volume
64pub_type
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