Colorectal cancer (CRC) is one of the major malignancies in humans. This study was designed to evaluate the effects of fucoidan on gut flora and tumor prevention in 1,2-dimethylhydrazine-induced colorectal carcinogenesis in rats. We found that dietary fucoidan treatment decreased the tumor incidence and mean tumor weight and increased cell apoptosis. Fucoidan treatment decreased the expression of β-catenin C-Myc, CyclinD1 and Survivin, while the Hippo pathway was activated with increased phosphorylation levels of mammalian sterile 20-like kinase 1 and 2, large tumor suppressor 1 and 2, and Yes-associated protein. Compared with the model group, the levels of interleukin (IL)-17 and IL-23 were decreased, but the levels of interferon-γ, IL-4 and IL-10 were increased, in the fucoidan group. Fucoidan treatment increased natural killer cells in peripheral blood and the proportion of CD4+ T cells. Immunofluorescence detection of colorectal tumor tissues showed decreased expression of Foxp3 and up-regulated expression of CD68 in the fucoidan group. Moreover, fucoidan treatment decreased the levels of diamine oxidase and lipopolysaccharides and up-regulated the levels of tight junction proteins. 16S rDNA high-throughput sequencing revealed that fucoidan treatment decreased the abundance of Prevotella and increased the abundance of Alloprevotella. Fucoidan increased the levels of butyric acid and valeric acid compared to the model group. This study provides experimental evidence that dietary fucoidan may prevent colorectal tumorigenesis by regulating gut microecology and body immunity. Meanwhile, fucoidan activated the Hippo pathway and down-regulated the β-catenin pathway to induce tumor cell apoptosis and suppress tumor growth.

大肠癌（CRC）是人类的主要恶性肿瘤之一。这项研究旨在评估岩藻依聚糖对1,2-二甲基肼诱导的大鼠大肠癌发生中肠道菌群和肿瘤预防的作用。我们发现饮食岩藻依聚糖治疗可降低肿瘤发生率和平均肿瘤重量并增加细胞凋亡。岩藻依丹治疗可降低β-cateninC-Myc，CyclinD1和Survivin的表达，而Hippo通路则被哺乳动物不育20样激酶1和2，大肿瘤抑制物1和2以及Yes相关蛋白的磷酸化水平提高所激活。 。在岩藻依聚糖组中，与模型组相比，白细胞介素（IL）-17和IL-23的水平降低，而干扰素-γ，IL-4和IL-10的水平升高。岩藻依丹治疗可增加外周血中的自然杀伤细胞和CD4 + T细胞的比例。大肠肿瘤组织的免疫荧光检测显示，岩藻依聚糖组中Foxp3的表达降低，而CD68的表达上调。此外，岩藻依聚糖处理降低了二胺氧化酶和脂多糖的水平，并上调了紧密连接蛋白的水平。16S rDNA高通量测序表明，岩藻依聚糖处理降低了沙门氏菌的丰度普雷沃和增加的丰度Alloprevotella。与模型组相比，褐藻糖胶增加了丁酸和戊酸的水平。这项研究提供了实验证据，表明岩藻依聚糖可以通过调节肠道微生态和机体免疫力来预防大肠癌的发生。同时，岩藻依聚糖激活了Hippo通路并下调了β-catenin通路，从而诱导肿瘤细胞凋亡并抑制了肿瘤的生长。