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Mol. Cells 2009; 28(2): 119-124

Published online August 20, 2009

https://doi.org/10.1007/s10059-009-0116-x

© The Korean Society for Molecular and Cellular Biology

Enhanced Cytotoxicity of 5-FU by bFGF through
Up-Regulation of Uridine Phosphorylase 1

Young-Sam Im, Hea Kyeong Shin, Hye-Ryun Kim, So-Hee Jeong, Seung-Ryul Kim,
Yong-Min Kim, Do Hyung Lee, Seong-Ho Jeon, Hyeon-Woo Lee, and Joong-Kook Choi

Received: June 11, 2009; Revised: July 7, 2009; Accepted: July 10, 2009

Abstract

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-α, IL1 and IFN-γ. 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.

Keywords 5-DFUR (= 5-dFURd), 5-FU, apoptosis, ATDC5 chondroprogenitor cells, bFGF, C2C12 pre-myoblasts, NF

Article

Research Article

Mol. Cells 2009; 28(2): 119-124

Published online August 31, 2009 https://doi.org/10.1007/s10059-009-0116-x

Copyright © The Korean Society for Molecular and Cellular Biology.

Enhanced Cytotoxicity of 5-FU by bFGF through
Up-Regulation of Uridine Phosphorylase 1

Young-Sam Im, Hea Kyeong Shin, Hye-Ryun Kim, So-Hee Jeong, Seung-Ryul Kim,
Yong-Min Kim, Do Hyung Lee, Seong-Ho Jeon, Hyeon-Woo Lee, and Joong-Kook Choi

Received: June 11, 2009; Revised: July 7, 2009; Accepted: July 10, 2009

Abstract

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-α, IL1 and IFN-γ. 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.

Keywords: 5-DFUR (= 5-dFURd), 5-FU, apoptosis, ATDC5 chondroprogenitor cells, bFGF, C2C12 pre-myoblasts, NF

Mol. Cells
Feb 28, 2023 Vol.46 No.2, pp. 69~129
COVER PICTURE
The bulk tissue is a heterogeneous mixture of various cell types, which is depicted as a skein of intertwined threads with diverse colors each of which represents a unique cell type. Single-cell omics analysis untangles efficiently the skein according to the color by providing information of molecules at individual cells and interpretation of such information based on different cell types. The molecules that can be profiled at the individual cell by single-cell omics analysis includes DNA (bottom middle), RNA (bottom right), and protein (bottom left). This special issue reviews single-cell technologies and computational methods that have been developed for the single-cell omics analysis and how they have been applied to improve our understanding of the underlying mechanisms of biological and pathological phenomena at the single-cell level.

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