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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
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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