Osteosarcoma (OS) is the most common pediatric bone cancer in children and young adults. Previous
studies have suggested the importance of osteoblast activity in OS tumorigenesis and metastasis, as OS is
characterized by abnormal bone formation, while osteoblast is the predominant cell type both in OS and in
metastatic tumor tissues. RUNX2 is a known essential transcription factor for osteoblast differentiation. RUNX2
has also been linked to many human cancers, including bone cancers and cancer metastasis in bone. However, the
view of RUNX2 during OS tumorigenesis has not been unanimous. In this manuscript, we reviewed the
osteoblastic origin in OS etiology. The oncogenic property of RUNX2 in human OS studies was briefly summarized. RUNX2 may be
involved in OS pathogenesis by regulating cell cycle controlling of (pre)-osteoblasts, which subsequently convert to OS cells. The roles
and mechanisms of RUNX2 during OS metastasis and bone metastasis in target cancers (herein prostate and breast cancers), were as
described. The potential involvement of Runx2 in multiple mouse OS models that use human OS cell lines (Xenografts), tumor
suppressor genes p53 and Rb1 were also discussed. Finally, we updated some microRNAs studies and their relation with RUNX2 in OS
pathogenesis. This review provides a comprehensive understanding of RUNX2’s function during OS pathogenesis and will help with the
research designing and strategy in controlling OS.
Keywords: Animal model, bone metastasis, microRNA, osteosarcoma, Runx2, tumorigenesis.
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