Szychowski Konrad A, Skóra Bartosz, Bar Monika, Piechowiak Tomasz
Department of Biotechnology and Cell Biology, Medical College, University of Information Technology and Management in Rzeszow, Sucharskiego 2, 35-225 Rzeszow, Poland.
Department of Biotechnology and Cell Biology, Medical College, University of Information Technology and Management in Rzeszow, Sucharskiego 2, 35-225 Rzeszow, Poland.
Biomed Pharmacother. 2022 May;149:112815. doi: 10.1016/j.biopha.2022.112815. Epub 2022 Mar 11.
The oral cancer is presumably caused by genetic factors and exposure to substances derived from cosmetics and disinfectants. Triclosan (TCS) is widely spread in many consumer products and oral care products. Since TCS can affect DNA methylation, which is one of the key mechanisms of gene expression that may lead to cancerogenesis, it is necessary to study this mechanism in oral cell carcinoma. The aim of the present study was to evaluate the impact of TCS on metabolic parameters, oxidative stress, gene expression, and DNA methylation and hydroxymethylation in the SCC-15 cell line. The experiments have shown TCS toxicity to SCC-15 cells only in the highest concentrations of 50 and 100 µM. TCS in a wide range of concentrations increases ROS production and caspase-3 activity. Our experiments have shown that TCS in the nontoxic concentrations of 10 µM exerts an impact on SOD2 mRNA expression and SOD activity in the SCC-15 cell line. Finally, our experiments have demonstrated that 6-h treatment with TCS decreases the mRNA expression of DNMT3A and DNMT3B. After 72-h exposure to TCS, an increased level of 5-methylcytosine and 5-hydroxymethylcytosine was observed in the SCC-15 cell line, but it was abolished by the NAC treatment. However, it is very likely that these results can be an effect of TET enzyme activity, especially in the case of the decrease in 5mC and the increase in 5hmC after the 48-h exposure to TCS, which was accompanied with a decrease in the mRNA expression of DNMT3A and DNMT3B.
口腔癌可能由遗传因素以及接触化妆品和消毒剂中的物质引起。三氯生（TCS）广泛存在于许多消费品和口腔护理产品中。由于TCS会影响DNA甲基化，而DNA甲基化是可能导致癌症发生的基因表达关键机制之一，因此有必要在口腔细胞癌中研究这一机制。本研究的目的是评估TCS对SCC - 15细胞系的代谢参数、氧化应激、基因表达以及DNA甲基化和羟甲基化的影响。实验表明，仅在最高浓度50和100 µM时TCS对SCC - 15细胞具有毒性。在很宽的浓度范围内，TCS会增加活性氧（ROS）的产生和半胱天冬酶 - 3的活性。我们的实验表明，无毒浓度10 µM的TCS会影响SCC - 15细胞系中SOD2 mRNA的表达和超氧化物歧化酶（SOD）的活性。最后，我们的实验证明，用TCS处理6小时会降低DNMT3A和DNMT3B的mRNA表达。在SCC - 15细胞系中，暴露于TCS 72小时后，观察到5 - 甲基胞嘧啶和5 - 羟甲基胞嘧啶水平升高，但用N - 乙酰半胱氨酸（NAC）处理后这种升高被消除。然而，这些结果很可能是TET酶活性的作用，特别是在暴露于TCS 48小时后5mC减少和5hmC增加的情况下，同时伴随着DNMT3A和DNMT3B的mRNA表达下降。
