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- Title
1,25(OH)<sub>2</sub>Vitamin D<sub>3</sub> induces elevated expression of the cell cycle inhibitor p18 in a squamous cell carcinoma cell line of the head and neck.
- Authors
Gedlicka, Claudia; Hager, Gudrun; Weissenböck, Martina; Gedlicka, Wilhelm; Knerer, Birgit; Kornfehl, Johannes; Formanek, Michael
- Abstract
Background: 1 α,25-Dihydroxyvitamin D3 [1,25(OH)2 Vitamin D3] induces growth inhibition in squamous cell carcinoma (SCC) cell lines of the head and neck by arresting the cells in the G0/G1 phase of the cell cycle, probably due to an enhanced expression of p21, which could be demonstrated in other cell lines (JPPA, SCC9) before. In SCC25, a SCC cell line isolated from tongue, growth inhibition but no overexpression of p21 was detected. The retinoblastoma gene, as a direct target of G1 cyclin–CDK complexes, showed an obvious shift from the hyperphosphorylated to the hypophosphorylated form under 1,25(OH)2Vitamin D3, which indicates that the growth inhibition takes place in the G0/G1 phase. To explore the possible pathway of growth inhibition in SCC25 we investigated other cell cycle inhibitors (p18, p19, p27). Methods: Synchronized cells were treated with 1,25(OH)2Vitamin D3 over 96 h. The cell cycle status and expression of cell cycle-regulating proteins was determined by fluorescence-activated cell sorting (FACS) and Western blotting. Results: An overexpression of p18 in 1,25(OH)2Vitamin D3 vs. ethanol-treated cells was determined until 30 h in SCC25. No influence was detectable on the expression of p27 and p19. Conclusion: One mechanism by which 1,25(OH)2Vitamin D3 controls cell growth might be the upregulation of p21. As p21 was unsusceptible to 1,25(OH)2Vitamin D3 in SCC25, other inhibiting proteins were necessary to be tested. The proven upregulation of p18 seems to be the responsible step for growth inhibition of 1,25(OH)2Vitamin D3 in SCC25.
- Subjects
CANCER; DISEASES; TUMORS; VITAMIN D; CALCIUM regulating hormones
- Publication
Journal of Oral Pathology & Medicine, 2006, Vol 35, Issue 8, p472
- ISSN
0904-2512
- Publication type
Article
- DOI
10.1111/j.1600-0714.2006.00407.x