双酚 B 暴露通过调节 C57BL/6J 小鼠的脂质代谢促进黑色素瘤的发展

IF 4.4 3区 医学 Q2 ENVIRONMENTAL SCIENCES
Xuening Ma, Qianchao Shao, Shuxian Huang, Weigao Zhang, Hu Liu, Xu Jiayi, Xunan Zhao, Peiqi Li, Da Shao, YuanQing Bu, Dan Weng
{"title":"双酚 B 暴露通过调节 C57BL/6J 小鼠的脂质代谢促进黑色素瘤的发展","authors":"Xuening Ma, Qianchao Shao, Shuxian Huang, Weigao Zhang, Hu Liu, Xu Jiayi, Xunan Zhao, Peiqi Li, Da Shao, YuanQing Bu, Dan Weng","doi":"10.1002/tox.24441","DOIUrl":null,"url":null,"abstract":"<p><p>The increasing incidence of cancer underscore the necessity of investigating contributors such as endocrine-disrupting chemicals (EDCs), including bisphenol A (BPA). Although BPA's risks are well-documented, comprehensive studies on its substitutes, such as bisphenol B (BPB), are limited. Dysregulated lipid metabolism is a hallmark of cancer progression. Our previous work demonstrated that BPA and bisphenol S (BPS) disrupt lipid metabolism via the peroxisome proliferator-activated receptor γ (PPARγ) pathway. We hence hypothesized that BPB might similarly perturb lipid metabolism and promote tumor growth. BPB's impact on lipid metabolism was investigated in vitro and in vivo using B16 melanoma cancer cells. Our findings indicate BPB exposure significantly increased lipid metabolism in B16 cells, enhancing cell proliferation and migration, and promoting tumor development in mice. Utilizing siRNA transfection or chemical inhibitor, we found that stearoyl-CoA desaturase-1 (SCD1), a key enzyme in lipid synthesis pathway, was required for BPB-induced lipid accumulation and cancer cell migration. Docking analysis revealed BPB may activate gene expression related to lipid metabolism and angiogenesis by interacting with PPARγ and hypoxia-inducible factor-1α (HIF-1α). This study illuminates BPB's potential role in advancing melanoma through lipid metabolism manipulation, highlighting the need for further research into the safety of BPA substitutes and their impact on cancer development.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4000,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Bisphenol B Exposure Promotes Melanoma Progression via Dysregulation of Lipid Metabolism in C57BL/6J Mice.\",\"authors\":\"Xuening Ma, Qianchao Shao, Shuxian Huang, Weigao Zhang, Hu Liu, Xu Jiayi, Xunan Zhao, Peiqi Li, Da Shao, YuanQing Bu, Dan Weng\",\"doi\":\"10.1002/tox.24441\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The increasing incidence of cancer underscore the necessity of investigating contributors such as endocrine-disrupting chemicals (EDCs), including bisphenol A (BPA). Although BPA's risks are well-documented, comprehensive studies on its substitutes, such as bisphenol B (BPB), are limited. Dysregulated lipid metabolism is a hallmark of cancer progression. Our previous work demonstrated that BPA and bisphenol S (BPS) disrupt lipid metabolism via the peroxisome proliferator-activated receptor γ (PPARγ) pathway. We hence hypothesized that BPB might similarly perturb lipid metabolism and promote tumor growth. BPB's impact on lipid metabolism was investigated in vitro and in vivo using B16 melanoma cancer cells. Our findings indicate BPB exposure significantly increased lipid metabolism in B16 cells, enhancing cell proliferation and migration, and promoting tumor development in mice. Utilizing siRNA transfection or chemical inhibitor, we found that stearoyl-CoA desaturase-1 (SCD1), a key enzyme in lipid synthesis pathway, was required for BPB-induced lipid accumulation and cancer cell migration. Docking analysis revealed BPB may activate gene expression related to lipid metabolism and angiogenesis by interacting with PPARγ and hypoxia-inducible factor-1α (HIF-1α). This study illuminates BPB's potential role in advancing melanoma through lipid metabolism manipulation, highlighting the need for further research into the safety of BPA substitutes and their impact on cancer development.</p>\",\"PeriodicalId\":11756,\"journal\":{\"name\":\"Environmental Toxicology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":4.4000,\"publicationDate\":\"2024-11-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Environmental Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1002/tox.24441\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/tox.24441","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0

摘要

癌症发病率的不断上升突出表明,有必要对包括双酚 A (BPA) 在内的干扰内分泌的化学品 (EDC) 等致癌物质进行调查。尽管双酚 A 的风险已得到充分证实,但对其替代品(如双酚 B (BPB))的全面研究却十分有限。脂质代谢失调是癌症发展的一个标志。我们之前的研究表明,双酚 A 和双酚 S(BPS)通过过氧化物酶体增殖激活受体γ(PPARγ)途径破坏脂质代谢。因此,我们推测 BPB 可能同样会扰乱脂质代谢并促进肿瘤生长。我们使用 B16 黑色素瘤癌细胞对 BPB 对脂质代谢的影响进行了体外和体内研究。我们的研究结果表明,暴露于 BPB 会明显增加 B16 细胞的脂质代谢,增强细胞增殖和迁移,促进小鼠肿瘤的发展。利用 siRNA 转染或化学抑制剂,我们发现硬脂酰-CoA 去饱和酶-1(SCD1)是脂质合成途径中的一个关键酶,是 BPB 诱导脂质积累和癌细胞迁移所必需的。对接分析表明,BPB 可通过与 PPARγ 和缺氧诱导因子-1α(HIF-1α)相互作用,激活与脂质代谢和血管生成相关的基因表达。这项研究揭示了 BPB 通过操纵脂质代谢在促进黑色素瘤发展方面的潜在作用,强调了进一步研究双酚 A 替代品的安全性及其对癌症发展的影响的必要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bisphenol B Exposure Promotes Melanoma Progression via Dysregulation of Lipid Metabolism in C57BL/6J Mice.

The increasing incidence of cancer underscore the necessity of investigating contributors such as endocrine-disrupting chemicals (EDCs), including bisphenol A (BPA). Although BPA's risks are well-documented, comprehensive studies on its substitutes, such as bisphenol B (BPB), are limited. Dysregulated lipid metabolism is a hallmark of cancer progression. Our previous work demonstrated that BPA and bisphenol S (BPS) disrupt lipid metabolism via the peroxisome proliferator-activated receptor γ (PPARγ) pathway. We hence hypothesized that BPB might similarly perturb lipid metabolism and promote tumor growth. BPB's impact on lipid metabolism was investigated in vitro and in vivo using B16 melanoma cancer cells. Our findings indicate BPB exposure significantly increased lipid metabolism in B16 cells, enhancing cell proliferation and migration, and promoting tumor development in mice. Utilizing siRNA transfection or chemical inhibitor, we found that stearoyl-CoA desaturase-1 (SCD1), a key enzyme in lipid synthesis pathway, was required for BPB-induced lipid accumulation and cancer cell migration. Docking analysis revealed BPB may activate gene expression related to lipid metabolism and angiogenesis by interacting with PPARγ and hypoxia-inducible factor-1α (HIF-1α). This study illuminates BPB's potential role in advancing melanoma through lipid metabolism manipulation, highlighting the need for further research into the safety of BPA substitutes and their impact on cancer development.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Environmental Toxicology
Environmental Toxicology 环境科学-毒理学
CiteScore
7.10
自引率
8.90%
发文量
261
审稿时长
4.5 months
期刊介绍: The journal publishes in the areas of toxicity and toxicology of environmental pollutants in air, dust, sediment, soil and water, and natural toxins in the environment.Of particular interest are: Toxic or biologically disruptive impacts of anthropogenic chemicals such as pharmaceuticals, industrial organics, agricultural chemicals, and by-products such as chlorinated compounds from water disinfection and waste incineration; Natural toxins and their impacts; Biotransformation and metabolism of toxigenic compounds, food chains for toxin accumulation or biodegradation; Assays of toxicity, endocrine disruption, mutagenicity, carcinogenicity, ecosystem impact and health hazard; Environmental and public health risk assessment, environmental guidelines, environmental policy for toxicants.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信