Valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin-1 expression
<p>Abstract</p> <p>Background</p> <p>Prevention of bladder cancer recurrence is a central challenge in the management of this highly prevalent disease. The histone deacetylase inhibitor valproic acid (sodium valproate) has anti-angiogenic properties and has been shown t...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2012-08-01
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| Series: | BMC Urology |
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| Online Access: | http://www.biomedcentral.com/1471-2490/12/21 |
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| author | Byler Timothy K Leocadio Dean Shapiro Oleg Bratslavsky Gennady Stodgell Christopher J Wood Ronald W Messing Edward M Reeder Jay E |
| author_facet | Byler Timothy K Leocadio Dean Shapiro Oleg Bratslavsky Gennady Stodgell Christopher J Wood Ronald W Messing Edward M Reeder Jay E |
| author_sort | Byler Timothy K |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>Prevention of bladder cancer recurrence is a central challenge in the management of this highly prevalent disease. The histone deacetylase inhibitor valproic acid (sodium valproate) has anti-angiogenic properties and has been shown to decrease bladder cancer growth in model systems. We have previously shown reduced expression of thrombospondin-1 in a mouse model and in human bladder cancer relative to normal urothelium. We speculated that inhibition of angiogenesis by valproate might be mediated by this anti-angiogenic protein.</p> <p>Methods</p> <p>Bladder cancer cell lines UMUC3 and T24 were treated with valproate or another histone deacetylase inhibitor, vorinostat, in culture for a period of three days. Proliferation was assessed by alamar blue reduction. Gene expression was evaluated by reverse transcription of RNA and quantitative PCR.</p> <p>Results</p> <p>Proliferation assays showed treatment with valproate or vorinostat decreased proliferation in both cell lines. Histone deacetylase inhibition also increased relative expression of thrombospondin-1 up to 8 fold at 5 mM valproate.</p> <p>Conclusions</p> <p>Histone deacetylase inhibitors warrant further study for the prevention or treatment of bladder cancer.</p> |
| first_indexed | 2024-12-18T04:18:14Z |
| format | Article |
| id | doaj.art-9b4aecc991cb447fbac457e8e110ee91 |
| institution | Directory Open Access Journal |
| issn | 1471-2490 |
| language | English |
| last_indexed | 2024-12-18T04:18:14Z |
| publishDate | 2012-08-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Urology |
| spelling | doaj.art-9b4aecc991cb447fbac457e8e110ee912022-12-21T21:21:18ZengBMCBMC Urology1471-24902012-08-011212110.1186/1471-2490-12-21Valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin-1 expressionByler Timothy KLeocadio DeanShapiro OlegBratslavsky GennadyStodgell Christopher JWood Ronald WMessing Edward MReeder Jay E<p>Abstract</p> <p>Background</p> <p>Prevention of bladder cancer recurrence is a central challenge in the management of this highly prevalent disease. The histone deacetylase inhibitor valproic acid (sodium valproate) has anti-angiogenic properties and has been shown to decrease bladder cancer growth in model systems. We have previously shown reduced expression of thrombospondin-1 in a mouse model and in human bladder cancer relative to normal urothelium. We speculated that inhibition of angiogenesis by valproate might be mediated by this anti-angiogenic protein.</p> <p>Methods</p> <p>Bladder cancer cell lines UMUC3 and T24 were treated with valproate or another histone deacetylase inhibitor, vorinostat, in culture for a period of three days. Proliferation was assessed by alamar blue reduction. Gene expression was evaluated by reverse transcription of RNA and quantitative PCR.</p> <p>Results</p> <p>Proliferation assays showed treatment with valproate or vorinostat decreased proliferation in both cell lines. Histone deacetylase inhibition also increased relative expression of thrombospondin-1 up to 8 fold at 5 mM valproate.</p> <p>Conclusions</p> <p>Histone deacetylase inhibitors warrant further study for the prevention or treatment of bladder cancer.</p>http://www.biomedcentral.com/1471-2490/12/21Bladder cancerValproic acidThrombospondin-1, Urothelial carcinomaGene expression |
| spellingShingle | Byler Timothy K Leocadio Dean Shapiro Oleg Bratslavsky Gennady Stodgell Christopher J Wood Ronald W Messing Edward M Reeder Jay E Valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin-1 expression BMC Urology Bladder cancer Valproic acid Thrombospondin-1, Urothelial carcinoma Gene expression |
| title | Valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin-1 expression |
| title_full | Valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin-1 expression |
| title_fullStr | Valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin-1 expression |
| title_full_unstemmed | Valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin-1 expression |
| title_short | Valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin-1 expression |
| title_sort | valproic acid decreases urothelial cancer cell proliferation and induces thrombospondin 1 expression |
| topic | Bladder cancer Valproic acid Thrombospondin-1, Urothelial carcinoma Gene expression |
| url | http://www.biomedcentral.com/1471-2490/12/21 |
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