<p>The vitamin D metabolite 1,25(OH)2D3 has long been known to inhibit growth of prostate cancer cells and this mainly through a VDR-mediated pathway controlling target gene expression, resulting in cell cycle arrest, apoptosis and differentiation. Another major way inwhich 1,25(OH)2D3 inhibits cell growth in prostate cancer is via membrane-initiated steroid signalling, which triggers activation of signal cascades upon steroid binding to a receptor complex, leading to induction of genes regulating cell growth, proliferation and apoptosis. The main prostate cancer inhibiting membrane-initiated route is the TGFβ signalling pathway, elicited by the protein TGFβ. Another important protein downstream in this cascade is Smad2. In this study the early effects of 1,25(OH)2D3 on activated Smad2 levels in PC-3 prostate cancer cells were examined. PC-3 cells were incubated for 5, 10, 30 and 60 minutes as well as 24 and 40 hours both together with 1,25(OH)2D3 of the concentrations 10-10 and 107 M and without. An ELISA assay scanning for activated Smad2 was then performed on supernatants from both treated and untreated cells. This is a follow-up to an earlier study which examined the influence of 1,25(OH)2D3 on TGFβ levels using the same doses and similar time points and which found that 1,25(OH)2D3 initially lowered the level of active TGFβ, then increased it. The results of this study showed a statistically insignificant, time delayed 1,25(OH)2D3 mediated induction of the same pattern in the levels of active Smad2.</p> / Project Work in Biomedicine, Advanced Level, 7.5 ECTS
| Identifer | oai:union.ndltd.org:UPSALLA/oai:DiVA.org:his-3807 |
| Date | January 2009 |
| Creators | Stahel, Anette |
| Publisher | University of Skövde, School of Life Sciences |
| Source Sets | DiVA Archive at Upsalla University |
| Language | English |
| Detected Language | English |
| Type | Student thesis, text |
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