Abstract:
:Previous studies have suggested that 1,25(OH)2D3, the active form of vitamin D3, may increase the survival of bone-forming osteoblasts through an inhibition of apoptosis. On the other hand, vitamin D3 has also been shown to trigger apoptosis in human cancer cells, including osteosarcoma-derived cell lines. In the present study, we show that 1,25(OH)2D3 induces a time- and dose-dependent loss of cell viability in the rat osteosarcoma cell line, UMR-106, and the human osteosarcoma cell line, TE-85. We were unable, however, to detect nuclear condensation, phosphatidylserine externalization, or other typical signs of apoptosis in this model. Moreover, 1,25(OH)2D3 failed to protect against apoptosis induced by serum starvation or incubation with the protein kinase inhibitor, staurosporine. These in vitro findings are thus at variance with several previous reports in the literature and suggest that induction of or protection against apoptosis of bone-derived cells may not be a primary function of vitamin D3.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Witasp E,Gustafsson AC,Cotgreave I,Lind M,Fadeel Bdoi
10.1016/j.bbrc.2005.03.061subject
Has Abstractpub_date
2005-05-13 00:00:00pages
891-7issue
3eissn
0006-291Xissn
1090-2104pii
S0006-291X(05)00529-2journal_volume
330pub_type
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