论文库首页  论文库
 
论文编号:
论文题目: Long-term di (2-ethylhexyl)-phthalate exposure promotes proliferation and survival of HepG2 cells via activation of NF kappa B
英文论文题目: Long-term di (2-ethylhexyl)-phthalate exposure promotes proliferation and survival of HepG2 cells via activation of NF kappa B
第一作者: Wei, N; Feng, XY; Xie, ZQ; Zhang, YA; Feng, Y
英文第一作者: Wei, N; Feng, XY; Xie, ZQ; Zhang, YA; Feng, Y
联系作者: Feng, Y (reprint author), 320 Yueyang Rd, Shanghai, Peoples R China.
英文联系作者: Feng, Y (reprint author), 320 Yueyang Rd, Shanghai, Peoples R China.
外单位作者单位:
英文外单位作者单位:
发表年度: 2017
卷: 42
期:
页码: 86-92
摘要: Di (2-ethylhexyl)-phthalate (DEHP) is the most commonly used plasticizer. DEHP can easily leach out from products into the environment and has become a significant environmental contamination. However, its carcinogenic effects in human remain controversial. In this study, we exposed hepatocellular carcinoma HepG2 cells to different concentrations of DEHP for a period of times, followed by a combination of RNA-seq analysis and molecular analysis for DEHP-altered genes. We observed that long-term and very low-dose DEHP treatment has growth-inducing activity in HepG2 cells, while short-term and high-dose DEHP treatment has little effects on tumor cell proliferation. Bioinformatic analysis further revealed that a large subset of differentially expressed genes affected by DEHP have functional annotations related to inflammation response. Importantly we found that long-term DEHP treatment stimulated nuclear factor-kappa B (NF-kappa B) activity in HepG2 cells, while inhibition of NF kappa B activity could offset the effects of DEHP exposure. In conclusion, continuous DEHP treatment could promote proliferation of HepG2 cells via activating NF kappa B signaling pathway.
英文摘要: Di (2-ethylhexyl)-phthalate (DEHP) is the most commonly used plasticizer. DEHP can easily leach out from products into the environment and has become a significant environmental contamination. However, its carcinogenic effects in human remain controversial. In this study, we exposed hepatocellular carcinoma HepG2 cells to different concentrations of DEHP for a period of times, followed by a combination of RNA-seq analysis and molecular analysis for DEHP-altered genes. We observed that long-term and very low-dose DEHP treatment has growth-inducing activity in HepG2 cells, while short-term and high-dose DEHP treatment has little effects on tumor cell proliferation. Bioinformatic analysis further revealed that a large subset of differentially expressed genes affected by DEHP have functional annotations related to inflammation response. Importantly we found that long-term DEHP treatment stimulated nuclear factor-kappa B (NF-kappa B) activity in HepG2 cells, while inhibition of NF kappa B activity could offset the effects of DEHP exposure. In conclusion, continuous DEHP treatment could promote proliferation of HepG2 cells via activating NF kappa B signaling pathway.
刊物名称: TOXICOLOGY IN VITRO
英文刊物名称: TOXICOLOGY IN VITRO
论文全文:
英文论文全文:
全文链接:
其它备注:
英文其它备注:
学科: Toxicology
英文学科: Toxicology
影响因子: 2.866
第一作者所在部门:
英文第一作者所在部门:
论文出处:
英文论文出处:
论文类别: Article
英文论文类别: Article
参与作者:
英文参与作者:
 
2014 中国科学院上海生命科学研究院 版权所有