Identification of genes induced by dibutyl phthalate in human thyroid follicular FTC-238 cells

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• 作者：Mee Song (1)
  Mi-Kyung Song (1)
  Han-Seam Choi (1)
  Ji-Seong Yoon (1)
  Chan-Young Shin (1)
  Hae-Yeon Choi (2)
  Youn-Jung Kim (3)
  Jae-Chun Ryu (1)
  
• 关键词：Dibutyl phthalate (DBP) ; Thyroid follicles ; Microarray ; Gene ontology (GO)
• 刊名：Toxicology and Environmental Health Sciences
• 出版年：2012
• 出版时间：June 2012
• 年：2012
• 卷：4
• 期：2
• 页码：80-86
• 全文大小：296KB
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• 作者单位：Mee Song (1)
  Mi-Kyung Song (1)
  Han-Seam Choi (1)
  Ji-Seong Yoon (1)
  Chan-Young Shin (1)
  Hae-Yeon Choi (2)
  Youn-Jung Kim (3)
  Jae-Chun Ryu (1)
  
  1. Cellular and Molecular Toxicology Laboratory, Korea Institute of Science & Technology, P.O. Box 131, Cheongryang, Seoul, 130-650, Korea
  2. Division of Food Sciences, Major in Foodservice Management and Nutririon, Kongju National University, Chungnam, 340-702, Korea
  3. Department of Food and Nutririon, College of Health Industry, Eulji University, Gyeonggi-do, 461-713, Korea
  
• ISSN：2233-7784

文摘

Dibutyl phthalates (DBP) are widely used as plasticizers to soften and increase the flexibility of polyvinyl chloride plastics, although they can leach into the surrounding environment. Many studies have reported that changes in thyroid function are linked to a variety of chemicals in the environment. Although the mechanism is not known, DBP decreases T3 and T4, and downregulates the sodium/iodide symporter promoter in the thyroid. We undertook a genome-wide analysis of transcriptional responses in human thyroid follicular carcinoma FTC-238 cells to non-toxic doses of DBP (100 μM). Whole human genome microarrays detected a total of 4,480 genes that exhibited altered expression after exposure to non-toxic doses of DBP compared with the vehicle control. We found that 2,218 and 2,262 genes showed different expression levels following treatment with non-toxic doses of DBP (1.5-fold (p <0.01)). Significant changes in the expression levels of multiple genes potentially critical in the regulation of DBP-induced thyroid disease were found. A DBP exposure gene network was identified and established by computational analysis. The possible roles of responsive genes and their related pathways during DBP treatment are discussed. This study details how cells respond to DBP exposure via transcriptional regulation. Information from our network could provide clues for further mechanistic studies that explain how DBP exposure leads to thyroid toxicity and disease.