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; Joong Kook Choi

doi:10.1007/s10059-009-0116-x

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
, Joong Kook Choi

Research output: Contribution to journal › Article › peer-review

17 Citations (Scopus)

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.

Original language	English
Pages (from-to)	119-124
Number of pages	6
Journal	Molecules and Cells
Volume	28
Issue number	2
DOIs	https://doi.org/10.1007/s10059-009-0116-x
Publication status	Published - 2009

Bibliographical note

Funding Information:
This work was supported by Korea Science and Engineering Foundation (KOSEF) Grant funded by the Korean Government (No. R01-2006-000-10030-0). This work was also supported by the GRRC project of Gyeonggi Provincial Government, Republic of Korea and by the research grant of the Chungbuk National University in 2006 to Joong-Kook Choi. We appreciate Arunku-mar for help in preparation of this manuscript.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

5-DFUR (= 5-dFURd)
5-FU
ATDC5 chondroprogenitor cells
Apoptosis
C2C12 pre-myoblasts
NFκB
Uridine phosphorylase
bFGF

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10.1007/s10059-009-0116-x

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@article{a8c54a25326e45bfb01b282306695143,

title = "Enhanced cytotoxicity of 5-FU by bFGF through up-regulation of uridine phosphorylase 1",

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, ATDC5 chondroprogenitor cells, Apoptosis, C2C12 pre-myoblasts, NFκB, Uridine phosphorylase, bFGF",

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

note = "Funding Information: This work was supported by Korea Science and Engineering Foundation (KOSEF) Grant funded by the Korean Government (No. R01-2006-000-10030-0). This work was also supported by the GRRC project of Gyeonggi Provincial Government, Republic of Korea and by the research grant of the Chungbuk National University in 2006 to Joong-Kook Choi. We appreciate Arunku-mar for help in preparation of this manuscript.",

year = "2009",

doi = "10.1007/s10059-009-0116-x",

language = "English",

volume = "28",

pages = "119--124",

journal = "Molecules and Cells",

issn = "1016-8478",

publisher = "Elsevier B.V.",

number = "2",

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TY - JOUR

T1 - Enhanced cytotoxicity of 5-FU by bFGF through up-regulation of uridine phosphorylase 1

AU - Im, Young Sam

AU - Shin, Hea Kyeong

AU - Kim, Hye Ryun

AU - Jeong, So Hee

AU - Kim, Seung Ryul

AU - Kim, Yong Min

AU - Lee, Do Hyung

AU - Jeon, Seong Ho

AU - Lee, Hyeon Woo

AU - Choi, Joong Kook

N1 - Funding Information: This work was supported by Korea Science and Engineering Foundation (KOSEF) Grant funded by the Korean Government (No. R01-2006-000-10030-0). This work was also supported by the GRRC project of Gyeonggi Provincial Government, Republic of Korea and by the research grant of the Chungbuk National University in 2006 to Joong-Kook Choi. We appreciate Arunku-mar for help in preparation of this manuscript.

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

KW - 5-DFUR (= 5-dFURd)

KW - 5-FU

KW - ATDC5 chondroprogenitor cells

KW - Apoptosis

KW - C2C12 pre-myoblasts

KW - NFκB

KW - Uridine phosphorylase

KW - bFGF

UR - https://www.scopus.com/pages/publications/69849116087

U2 - 10.1007/s10059-009-0116-x

DO - 10.1007/s10059-009-0116-x

M3 - Article

C2 - 19714313

AN - SCOPUS:69849116087

SN - 1016-8478

VL - 28

SP - 119

EP - 124

JO - Molecules and Cells

JF - Molecules and Cells

IS - 2

ER -

Enhanced cytotoxicity of 5-FU by bFGF through up-regulation of uridine phosphorylase 1

Abstract

Bibliographical note

UN SDGs

Keywords

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