Vitamin D decreases tumor cell growth and invasiveness in primary malignant bone tumors in vitro
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Updated: Aug 15, 2026
Isolation of Mesenchymal Stem Cells from Human Alveolar Periosteum and Effects of Vitamin D on Osteogenic Activity of Periosteum-derived Cells
Published on: May 4, 2018
1University of Würzburg, Department of Musculoskeletal Tissue Regeneration, Orthopedic Hospital König-Ludwig-Haus, Friedrich-Bergius-Ring 15, 97076 Würzburg, Germany.
Abstract:
Primary malignant bone tumors (PMBTs) are rare neoplasms arising from bone tissue. Limited evidence suggests an association between reduced serum 25(OH) vitamin D3 levels and PMBT incidence. The active metabolite 1,25(OH)2 vitamin D3 (1,25D3) modulates tumor cell proliferation, apoptosis, and migration through interactions with the vitamin D receptor (VDR). This study investigated the effects of 1,25D3 on osteosarcoma (MG-63, SaOS-2), chondrosarcoma (SW-1353), and Ewing's sarcoma (RD-ES) cell lines. Expression of key components of vitamin D metabolism, including 1α-hydroxylase (CYP27B1), 24-hydroxylase (CYP24A1), VDR, protein disulfide-isomerase A3 (PDIA3), and the 1,25D3-responsive bone gamma-carboxyglutamate protein (BGLAP), was analyzed at mRNA and protein levels. VDR nuclear translocation was assessed by Western blotting. Cell viability, cell cycle progression, apoptosis, and migration were evaluated using metabolic assays, flow cytometry, immunocytochemistry, wound healing, and live-cell imaging. Treatment with 1,25D3 upregulated CYP24A1 in osteosarcoma cells, while BGLAP expression was detected in both osteosarcoma and SW-1353 cells. All examined cell lines expressed VDR and PDIA3, and 1,25D3 induced VDR nuclear translocation. MG-63 cell viability decreased by 23%, whereas SW-1353 cell viability decreased by 10%, with no significant changes observed in SaOS-2 and RD-ES cells. In MG-63 cells, 1,25D3 induced a significant accumulation of cells in the G1 phase, consistent with cell-cycle arrest, whereas only minor cell-cycle alterations were observed in the other cell lines. Interestingly, 1,25D3 reduced the proportion of apoptotic osteosarcoma cells by 18-30%. The migration of MG-63 cells was significantly reduced by 1,25D3, and an inhibitory trend, albeit not statistically significant, was also observed in RD-ES cells. In conclusion, 1,25D3 modulated cell viability, apoptosis, and migration in PMBT cell models, with distinct, cell-type-specific responses. These findings suggest a potential role for 1,25D3 in regulating PMBT growth and invasiveness.
Insights
The active form of vitamin D, 1,25(OH)2 vitamin D3 (1,25D3), impacts primary malignant bone tumor (PMBT) cell behavior. This study shows 1,25D3 can reduce cancer cell viability and migration in specific PMBT models.
Area of Science:
- Oncology
- Endocrinology
- Molecular Biology
Background:
- Primary malignant bone tumors (PMBTs) are rare and their pathogenesis is not fully understood.
- Reduced vitamin D levels may be linked to increased PMBT incidence.
- The active vitamin D metabolite, 1,25(OH)2 vitamin D3 (1,25D3), influences cell processes relevant to cancer, such as proliferation and apoptosis, via the vitamin D receptor (VDR).
Purpose of the Study:
- To investigate the effects of 1,25D3 on different types of PMBT cell lines: osteosarcoma (MG-63, SaOS-2), chondrosarcoma (SW-1353), and Ewing's sarcoma (RD-ES).
- To analyze the expression of key vitamin D metabolism and signaling components within these cell lines.
- To evaluate how 1,25D3 treatment affects cell viability, cell cycle, apoptosis, and migration.
Main Methods:
- Cultured human PMBT cell lines (osteosarcoma, chondrosarcoma, Ewing's sarcoma).
- Analyzed mRNA and protein expression of vitamin D-related genes (CYP27B1, CYP24A1, VDR, PDIA3, BGLAP).
- Assessed VDR nuclear translocation, cell viability (metabolic assays), cell cycle (flow cytometry), apoptosis (immunocytochemistry), and migration (wound healing, live-cell imaging) after 1,25D3 treatment.
Main Results:
- 1,25D3 upregulated CYP24A1 in osteosarcoma cells and induced VDR nuclear translocation in all cell lines.
- MG-63 cell viability decreased by 23% and SW-1353 by 10%; MG-63 cells showed G1 phase cell-cycle arrest.
- 1,25D3 reduced apoptosis in osteosarcoma cells by 18-30% and significantly decreased migration in MG-63 cells.
Conclusions:
- 1,25D3 demonstrates cell-type-specific effects on PMBT cell viability, apoptosis, and migration.
- The findings suggest a potential role for 1,25D3 in modulating the growth and invasiveness of primary malignant bone tumors.
- Further research into vitamin D's role in bone cancer could inform therapeutic strategies.
