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 (TNFa, 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.

中文翻译：

---

萝卜硫烷对小鼠艾氏实体瘤的抗癌作用相关的分子变化

萝卜硫烷（SFN）的抗癌作用是由几种信号通路介导的。但是，关于小鼠艾氏实体瘤（EST）的潜在机制知之甚少。进行该研究以确定与SFN的抗癌作用相关的分子变化，并比较其预防（共治疗）和治疗（后治疗）作用。选择艾氏（鼠乳腺腺癌）实体瘤，并通过实时聚合酶链反应确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及其下游目标（HO1和CAT）的表达。）。相反，SFN给药会降低表观遗传相关基因（HDAC1和DNMT1）和炎症相关基因（TNFa，NFkB和Cox2）的表达。总体而言，SFN共处理比后处理策略具有明显的分子变化。这些数据表明，与SFN对EST的抗癌作用相关的分子变化涉及诱导氧化应激，抑制炎症和表观遗传修饰。