Journal
MOLECULES AND CELLS
Volume 28, Issue 2, Pages 119-124Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
DOI: 10.1007/s10059-009-0116-x
Keywords
5-DFUR (=5-dFURd); 5-FU; apoptosis; ATDC5 chondroprogenitor cells; bFGF; C2C12 pre-myoblasts; NF kappa B; uridine phosphorylase
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Funding
- Korean Government [R01-2006-000-10030-0]
- Gyeonggi Provincial Government, Republic of Korea
- Chungbuk National University
- National Research Foundation of Korea [R01-2006-000-10030-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Anti cancer agent 5-FU (Fluoro Uracil) is a prodrug that can be metabolized and then activated to interfere with RNA and DNA homeostasis. However, the majority of administered 5-FU is known to be catabolized in vivo in the liver where Dihydropyrimidine dehydrogenase (DPD) is abundantly expressed to degrade 5-FU. The biological factors that correlate with the response to 5-FU-based chemotherapy have been proposed to include uridine phosphorylase (UPP), thymidine phosphorylase (TPP), p53 and microsatellite instability. Among these, the expression of UPP is known to be controlled by cytokines such as TNF-alpha, IL1 and IFN-gamma. Our preliminary study using a DNA microarray technique showed that basic fibroblast growth factor (bFGF) markedly induced the expression of UPP1 at the transcription level. In the present study, we investigated whether bFGF could modulate the expression of UPP1 in osteo-lineage cells and examined the sensitivity of these cells to 5-FU mediated apoptosis.
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