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苯并(a)芘诱导HT - 29人结肠癌细胞的细胞毒性、细胞增殖、DNA损伤及基因表达谱改变。

Benzo(a)pyrene-induced cytotoxicity, cell proliferation, DNA damage, and altered gene expression profiles in HT-29 human colon cancer cells.

作者信息

Myers Jeremy N, Harris Kelly L, Rekhadevi Perumalla V, Pratap Siddharth, Ramesh Aramandla

机构信息

Department of Biochemistry, Cancer Biology, Neuroscience & Pharmacology, Meharry Medical College, 1005 D.B. Todd Blvd., Nashville, TN, 37208, USA.

Department of Biotechnology, St. Francis College for Women, Hyderabad, Telangana, 500016, India.

出版信息

Cell Biol Toxicol. 2021 Dec;37(6):891-913. doi: 10.1007/s10565-020-09579-5. Epub 2021 Jan 7.

Abstract

In the US alone, around 60,000 lives/year are lost to colon cancer. In order to study the mechanisms of colon carcinogenesis, in vitro model systems are required in addition to in vivo models. Towards this end, we have used the HT-29 colon cancer cells, cultured in Dulbecco's Modified Eagle Medium (DMEM), which were exposed to benzo(a)pyrene (BaP), a ubiquitous and prototypical environmental and dietary toxicant at 1, 10, 100 nM and 1, 5, 10, and 25 μM concentrations for 96 h. Post-BaP exposure, growth, cytotoxicity, apoptosis, and cell cycle changes were determined. The BaP metabolite concentrations in colon cells were identified and measured. Furthermore, the BaP biotransformation enzymes were studied at the protein and mRNA levels. The BaP exposure-induced damage to DNA was assessed by measuring the oxidative damage to DNA and the concentrations of BaP-DNA adducts. To determine the whole repertoire of genes that are up- or downregulated by BaP exposure, mRNA transcriptome analysis was conducted. There was a BaP exposure concentration (dose)-dependent decrease in cell growth, cytotoxicity, and modulation of the cell cycle in the treatment groups compared to untreated or dimethylsulfoxide (DMSO: vehicle for BaP)-treated categories. The phase I biotransformation enzymes, CYP1A1 and 1B1, showed BaP concentration-dependent expression. On the other hand, phase II enzymes did not exhibit any marked variation. Consistent with the expression of phase I enzymes, elevated concentrations of BaP metabolites were generated, contributing to the formation of DNA lesions and stable DNA adducts, which were also BaP concentration-dependent. In summary, our studies established that biotransformation of BaP contributes to cytotoxicity, proliferation of tumor cells, and alteration of gene expression by BaP. • Benzo(a)pyrene (BaP) is an environmental and dietary toxicant. • BaP causes cytotoxicity in cultured HT-29 colon cancer cells. • mRNA transcriptome analyses revealed that BaP impacts cell growth, cell cycle, biotransformation, and DNA damage.

摘要

仅在美国,每年就有大约6万人死于结肠癌。为了研究结肠癌发生的机制,除了体内模型外,还需要体外模型系统。为此,我们使用了在杜尔贝科改良伊格尔培养基(DMEM)中培养的HT-29结肠癌细胞,将其暴露于苯并(a)芘(BaP)中,BaP是一种普遍存在的典型环境和饮食毒物,浓度分别为1、10、100 nM以及1、5、10和25 μM,暴露96小时。BaP暴露后,测定细胞生长、细胞毒性、凋亡和细胞周期变化。鉴定并测量结肠细胞中BaP代谢物的浓度。此外,还在蛋白质和mRNA水平上研究了BaP生物转化酶。通过测量DNA的氧化损伤和BaP-DNA加合物的浓度来评估BaP暴露诱导的DNA损伤。为了确定因BaP暴露而上调或下调的基因的完整清单,进行了mRNA转录组分析。与未处理或用二甲基亚砜(DMSO:BaP的溶剂)处理的组相比,处理组中细胞生长、细胞毒性和细胞周期调节呈现出BaP暴露浓度(剂量)依赖性降低。I相生物转化酶CYP1A1和1B1呈现出BaP浓度依赖性表达。另一方面,II相酶没有表现出任何明显变化。与I相酶的表达一致,产生了浓度升高的BaP代谢物,导致DNA损伤和稳定的DNA加合物的形成,这也呈BaP浓度依赖性。总之,我们的研究表明,BaP的生物转化导致细胞毒性、肿瘤细胞增殖以及BaP引起的基因表达改变。• 苯并(a)芘(BaP)是一种环境和饮食毒物。• BaP在培养的HT-29结肠癌细胞中引起细胞毒性。• mRNA转录组分析表明,BaP影响细胞生长、细胞周期、生物转化和DNA损伤。

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