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Molecular changes associated with the anticancer effect of sulforaphane against Ehrlich solid tumour in mice

机译:与小鼠EHRLICH固体瘤的嗜睡效果相关的分子变化

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The anticancer effect of sulforaphane (SFN) is mediated by several signalling pathways. However, little is known regarding the underlying mechanism in Ehrlich solid tumours (ESTs) in mice. This study was conducted to determine molecular changes associated with the anticancer effect of SFN and to compare its preventive (cotreatment) and therapeutic (posttreatment) effects. Ehrlich (murine mammary adenocarcinoma) solid tumour was selected and changes in the gene expression were determined in tumour tissues by the real-time polymerase chain reaction. The results showed that SFN increased the expression of the oxidative stress gene NrF2 and its downstream targets (HO1 and CAT). Conversely, SFN administration decreased the expression of the epigenesis-related genes (HDAC1 and DNMT1) and inflammation-related genes (TNFα, NFkB and Cox2). Overall, SFN cotreatment presented notable molecular changes than the posttreatment strategy. These data suggest that molecular changes associated with the anticancer effects of SFN against EST involved induction of oxidative stress, inhibition of inflammation and epigenetic modifications.
机译:萝卜硫素(SFN)的抗癌作用是通过多种信号途径介导的。然而,关于小鼠埃利希实体瘤(EST)的潜在机制知之甚少。本研究旨在确定与SFN抗癌作用相关的分子变化,并比较其预防(联合治疗)和治疗(后治疗)效果。选择Ehrlich(小鼠乳腺癌)实体瘤,通过实时聚合酶链反应测定肿瘤组织中基因表达的变化。结果表明,SFN增加了氧化应激基因NrF2及其下游靶点(HO1和CAT)的表达。相反,服用SFN会降低表观基因(HDAC1和DNMT1)和炎症相关基因(TNFα、NFkB和Cox2)的表达。总的来说,与后处理策略相比,SFN联合处理呈现出显著的分子变化。这些数据表明,与SFN对EST的抗癌作用相关的分子变化涉及氧化应激诱导、炎症抑制和表观遗传修饰。

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