文化大學機構典藏 CCUR:Item 987654321/22951
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://irlib.pccu.edu.tw/handle/987654321/22951


    题名: The down-regulation of galectin-1 expression is a specific biomarker of arsenic toxicity
    作者: Chang, Yu-Ying
    Chiang, Ming-Chang
    Kuo, Tai-Chih
    Chi, Li-Ling
    Kao, Yung-Hsi
    Huang, Rong-Nan
    贡献者: 生物科技研究所
    关键词: BINDING-PROTEINS
    ACUTE PROMYELOCYTIC LEUKEMIA
    HAMSTER OVARY CELLS
    ACTIVATED RAT MACROPHAGES
    RNA INTERFERENCE
    DRINKING-WATER
    TRIOXIDE AS2O3
    LYMPHOBLASTOID-CELLS
    FUNCTIONAL-ANATOMY
    CLINICAL-EFFICACY
    日期: 2011-08-10
    上传时间: 2012-09-07 15:40:10 (UTC+8)
    摘要: Galectin-1 (GAL1) is known as a beta-galactoside-binding protein that also can bind with arsenic to regulate cell functions. Using RNA interference technique, we investigated the possible mechanism. involved in GAL1 modulation of arsenite-inhibited cell survival in 3T3 fibroblast and KB oral cancer cells. GAL1 gene knockdown significantly attenuated sodium arsenite (NaAsO(2)) and arsenic trioxide (As(2)O(3)) inhibition of cell survival. However, GAL1 gene knockdown did not alter the inhibition of cell survival by antimony chloride, cadmium chloride or nickel sulfate. These results suggested the GAL1 selectively affects particular types of heavy metal elements. Flow cytometric analysis indicated GAL1 gene knockdown also suppressed As(III)-stimulated levels of sub-G1 and G2/M growth arrest in both cells. Moreover, atomic absorption spectrophotometric results showed that GAL1 gene knockdown reduced the total arsenic accumulation of both cells after the NaAsO(2) and As(2)O(3) treatment. These results suggested that GAL1 gene knockdown mediates the apoptotic effects of arsenic in 3T3 and KB cells via regulation of the cellular arsenic levels. We propose that down-regulation of GAL1 expression may be a useful and specific biomarker in assessing the toxicity of arsenic exposure. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
    關聯: TOXICOLOGY LETTERS Volume: 205 Issue: 1 Pages: 38-46
    显示于类别:[生物科技研究所 ] 期刊論文

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