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首页> 外文期刊>RSC Advances >Niclosamide induces colorectal cancer apoptosis, impairs metastasis and reduces immunosuppressive cells in vivo
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Niclosamide induces colorectal cancer apoptosis, impairs metastasis and reduces immunosuppressive cells in vivo

机译：Niclosamide诱导结直肠癌凋亡，损害转移并减少体内免疫抑制细胞

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摘要

Colorectal cancer (CRC) is one of the most common malignancies with considerable metastatic potential, explaining the need for new candidates that inhibit tumor growth and metastasis. Constitutive activation of signal transducers and activator of transcription 3 (Stat3) signaling promote tumorigenesis through disordering of the expression of key genes, and is associated with CRC progression. In this study, niclosamide, an FDA approved anthelmintic drug identified as a potent inhibitor of Stat3, was assessed for its anti-CRC activities in vitro and in vivo. We showed that niclosamide significantly inhibited proliferation in four CRC cell lines. In addition, the apoptosis was also found after treatment with niclosamide, which was related with the up-regulation of cleaved-caspases-3 and Bax but the downregulation of Bcl-2 and the loss of mitochondrial membrane potential (Delta psi(m)) in CT26 cells. Moreover, niclosamide potently suppressed cell migration and invasion in a dose-dependent manner. Furthermore, our study showed that the administration of niclosamide in vivo markedly inhibited the number of tumor nodules in the abdomen metastasis model of colon cancer. The antitumor effect of niclosamide was correlated with a marked decrease in the number of MDSCs in tumor. Interestingly, niclosamide also suppressed the activation of FAK, Stat3 and the expression of matrix metalloproteinase MMP9. Taken together, these findings indicated that niclosamide might be a candidate drug for impairing the metastasis of colon cancer in part by inhibiting the activation of Stat3.
机译：结肠直肠癌（CRC）是具有相当常见的转移性潜力的恶性肿瘤之一，旨在抑制肿瘤生长和转移的新候选者的需求。术语旋转器和转录激活剂的组成型激活3（stat3）信号传导通过关键基因表达的疾病促进肿瘤引起，与CRC进展相关。在该研究中，Niclosamide，FDA批准的鉴定为Stat3的有效抑制剂的FDA批准的Zhelmintic药物，在体外和体内评估其抗CRC活性。我们表明，Niclosamide在四种CRC细胞系中显着抑制增殖。此外，在用萘酰胺处理后还发现细胞凋亡，其与切割的 - 胱天冬酶-3和Bax的上调相关，但是Bcl-2的下调和线粒体膜电位的损失（Delta psi（m））在CT26细胞中。此外，Niclosamide以剂量依赖性方式纯度抑制细胞迁移和侵袭。此外，我们的研究表明，体内Niclosamide施用显着抑制结肠癌腹部转移模型中的肿瘤结节数。 Niclosamide的抗肿瘤效应与肿瘤中MDSC的数量的显着降低相关。有趣的是，Niclosamide还抑制了FAK，STAT3和基质金属蛋白酶MMP9的表达的激活。在一起，这些发现表明，Niclosamide可以是用于抑制STAT3的活化的候选药物，用于抑制STAT3的活化。

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  • 来源
    《RSC Advances》 |2016年第107期|共12页
  • 作者

    Yang Fangfang; Ye Tinghong; Liu Zhihao; Fang Aiping; Luo Yi; Wei Wei; Li Yujue; Li Yali; Zeng Anqi; Deng Yuanle; Gou Hongfeng; Xie Yongmei; Zhang Yiwen; Wei Yuquan;

  • 作者单位

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Med Sch West China Hosp Dept Abdominal Canc Canc Ctr Chengdu Peoples R China;

    Sichuan Univ West China Med Sch Sch Publ Hlth Dept Food Hyg &

    Nutr Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Med Sch Sch Publ Hlth Dept Food Hyg &

    Nutr Chengdu Peoples R China;

    Sichuan Univ West China Med Sch West China Hosp Dept Abdominal Canc Canc Ctr Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

    Sichuan Univ West China Hosp State Key Lab Biotherapy Dept Liver Surg Chengdu Peoples R China;

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