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4-nitrophenol exposure in T24 human bladder cancer cells promotes proliferation, motilities, and epithelial-to-mesenchymal transition.
Environmental and Molecular Mutagenesis ( IF 2.8 ) Pub Date : 2019-10-26 , DOI: 10.1002/em.22345
Fulu Dong 1 , Lu Chen 1 , Rui Wang 1 , Weiping Yang 1 , Tingting Lu 1 , Yonghui Zhang 1
Affiliation  

Although health hazards of 4-nitrophenol (PNP) exposure have been reported, the adverse effects of PNP exposure on cancer biological features are still unknown. We investigated the effects of administration of PNP in T24 human bladder cancer cells. The results showed that PNP exposure promoted cellular proliferation, migration and invasion, inhibited adhesion and apoptosis in vitro. Using quantitative real-time PCR, we found that (1) the mRNA expression levels of cell-cycle regulators PCNA, cyclin D1 and COX-2 were increased in PNP-treated cells compared to controls, however, that of pro-apoptotic gene Bax was decreased; (2) the expression level of EMT-associated gene E-cadherin was decreased in PNP-treated cells, whereas those of N-cadherin, vimentin, snail, and slug were increased; (3) the expression levels of cancer-promoting genes HIF-1, IL-1β, VEGFα and K-Ras were enhanced, but those of tumor suppressors p53, PTEN and BRCA were decreased. There was a positive association between PNP exposure times and the promotion effects. Finally, we found that the expression level of PPARγ (γ1 isoform) was increased in PNP-treated T24 cells. GW9662, a specific PPARγ antagonist, attenuated PNP-induced cell migration and invasion. These findings indicate that PNP exposure may promote bladder cancer growth and progression involving PPARγ signaling. PPARγ is a potential target for development of novel intervention study on environment pollution. Environ. Mol. Mutagen. 2019. © 2019 Wiley Periodicals, Inc.

中文翻译:

T24人膀胱癌细胞中的4-硝基苯酚暴露可促进增殖,迁移和上皮向间充质转化。

尽管已经报道了4-硝基苯酚(PNP)暴露对健康的危害,但仍不清楚PNP暴露对癌症生物学特征的不利影响。我们调查了在T24人膀胱癌细胞中施用PNP的效果。结果表明,PNP暴露促进体外细胞增殖,迁移和侵袭,抑制粘附和凋亡。使用定量实时PCR,我们发现(1)与对照组相比,PNP处理的细胞中细胞周期调节因子PCNA,cyclin D1和COX-2的mRNA表达水平增加,但是促凋亡基因Bax减少了;(2)在PNP处理的细胞中,EMT相关基因E-钙粘蛋白的表达水平降低,而N-钙粘蛋白,波形蛋白,蜗牛和的表达水平升高。(3)癌促进基因HIF-1,IL-1β的表达水平;VEGFα和K-Ras增强,但抑癌p53,PTEN和BRCA的表达降低。PNP暴露时间与促进效果之间存在正相关。最后,我们发现在PNP处理的T24细胞中,PPARγ(γ1亚型)的表达水平升高。特异性PPARγ拮抗剂GW9662减弱了PNP诱导的细胞迁移和侵袭。这些发现表明,PNP暴露可能促进膀胱癌的生长和涉及PPARγ信号传导的进展。PPARγ是发展新型环境污染干预研究的潜在目标。环境。大声笑 诱变剂。2019.©2019 Wiley Periodicals,Inc. 我们发现PNP处理的T24细胞中PPARγ(γ1亚型)的表达水平升高。特异性PPARγ拮抗剂GW9662减弱了PNP诱导的细胞迁移和侵袭。这些发现表明,PNP暴露可能促进膀胱癌的生长和涉及PPARγ信号传导的进展。PPARγ是发展新型环境污染干预研究的潜在目标。环境。大声笑 诱变剂。2019.©2019 Wiley Periodicals,Inc. 我们发现PNP处理的T24细胞中PPARγ(γ1亚型)的表达水平升高。特异性PPARγ拮抗剂GW9662减弱了PNP诱导的细胞迁移和侵袭。这些发现表明,PNP暴露可能促进膀胱癌的生长和涉及PPARγ信号传导的进展。PPARγ是发展新型环境污染干预研究的潜在目标。环境。大声笑 诱变剂。2019.©2019 Wiley Periodicals,Inc. 环境。大声笑 诱变剂。2019.©2019 Wiley Periodicals,Inc. 环境。大声笑 诱变剂。2019.©2019 Wiley Periodicals,Inc.
更新日期:2020-03-20
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