Global S&T Development Trend Analysis Platform of Resources and Environment
DOI | 10.1289/EHP2698 |
Effects of Neonicotinoid Pesticides on Promoter-Specific Aromatase (CYP19) Expression in Hs578t Breast Cancer Cells and the Role of the VEGF Pathway | |
Caron-Beaudoin, Elyse1,2; Viau, Rachel1; Sanderson, J. Thomas1 | |
2018-04-01 | |
发表期刊 | ENVIRONMENTAL HEALTH PERSPECTIVES
![]() |
ISSN | 0091-6765 |
EISSN | 1552-9924 |
出版年 | 2018 |
卷号 | 126期号:4 |
文章类型 | Article |
语种 | 英语 |
国家 | Canada |
英文摘要 | BACKGROUND: Aromatasc (CYP19) is a key enzyme in estrogens biosynthesis. In the mammary gland, CYP19 gene is expressed at low levels under the regulation of its I.4 promoter. In hormone-dependent breast cancer, fibroblast cells surrounding the tumor express increased levels of CYP19 mRNA due to a decrease of I.4 promoter activity and an increase of PII, I.3, and I.7 promoter activity. Little is known about the effects of environmental chemicals on the promoter-specific CYP19 expression. OBJECTIVE: We aimed to determine the effects of two neonicotinoids (thiacloprid and imidacloprid) on promoter-specific CYP19 expression in Hs578t breast cancer cells and understand the signaling pathways involved. METHODS: Hs578t cells were exposed to various signaling pathway stimulants or neonicotinoids for 24 h. Promoter-specific expression of CYP19 was determined by real-time quantitative polymerase chain reaction and catalytic activity of aromatase by tritiated water release assay. RESULTS: To our knowledge, we are the first to demonstrate that the normal I.4 promoter and the breast cancer-relevant PII I.3, and I.7 promoters of CYP19 are active in these cells. We found that the expression of CYP19 via promoters PII, I.3, and I.7 in Hs578t cells was, in part, dependent on the activation of two VEGF signaling pathways: mitogen-activated protein kinase (MAPK) 1/3 and phospholipase C (PLC). Exposure of Hs578t cells to environmental concentrations of imidacloprid and thiacloprid resulted in a switch in CYP19 promoter usage, involving inhibition of I.4 promoter activity and an increase of PII, I.3, and I.7 promoter-mediated CYP19 expression and aromatase catalytic activity. Greater effects were seen at lower concentrations. Our results suggest that thiacloprid and imidacloprid exert their effects at least partially by inducing the MAPK 1/3 and/or PLC pathways. CONCLUSIONS: We demonstrated in vitro that neonicotinoids may stimulate a change in CYP19 promoter usage similar to that observed in patients with hormone-dependent breast cancer. |
领域 | 资源环境 |
收录类别 | SCI-E |
WOS记录号 | WOS:000431396900012 |
WOS关键词 | ENDOTHELIAL GROWTH-FACTOR ; ENDOCRINE-DISRUPTING CHEMICALS ; ADRENOCORTICAL CARCINOMA-CELLS ; ESTROGEN BIOSYNTHESIS ; SIGNALING PATHWAYS ; QUANTITATIVE-ANALYSIS ; PROSTAGLANDIN E-2 ; FEMALE RATS ; CYCLIC-AMP ; P450 GENE |
WOS类目 | Environmental Sciences ; Public, Environmental & Occupational Health ; Toxicology |
WOS研究方向 | Environmental Sciences & Ecology ; Public, Environmental & Occupational Health ; Toxicology |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/22712 |
专题 | 资源环境科学 |
作者单位 | 1.Univ Quebec, INRS Inst Armand Frappier, Laval, PQ, Canada; 2.Univ Montreal, Sch Publ Hlth, Dept Occupat & Environm Hlth, Montreal, PQ, Canada |
推荐引用方式 GB/T 7714 | Caron-Beaudoin, Elyse,Viau, Rachel,Sanderson, J. Thomas. Effects of Neonicotinoid Pesticides on Promoter-Specific Aromatase (CYP19) Expression in Hs578t Breast Cancer Cells and the Role of the VEGF Pathway[J]. ENVIRONMENTAL HEALTH PERSPECTIVES,2018,126(4). |
APA | Caron-Beaudoin, Elyse,Viau, Rachel,&Sanderson, J. Thomas.(2018).Effects of Neonicotinoid Pesticides on Promoter-Specific Aromatase (CYP19) Expression in Hs578t Breast Cancer Cells and the Role of the VEGF Pathway.ENVIRONMENTAL HEALTH PERSPECTIVES,126(4). |
MLA | Caron-Beaudoin, Elyse,et al."Effects of Neonicotinoid Pesticides on Promoter-Specific Aromatase (CYP19) Expression in Hs578t Breast Cancer Cells and the Role of the VEGF Pathway".ENVIRONMENTAL HEALTH PERSPECTIVES 126.4(2018). |
条目包含的文件 | 条目无相关文件。 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论