首页> 美国卫生研究院文献>Molecules >In Vivo Anti-Cancer Mechanism of Low-Molecular-Weight Fucosylated Chondroitin Sulfate (LFCS) from Sea Cucumber Cucumaria frondosa
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In Vivo Anti-Cancer Mechanism of Low-Molecular-Weight Fucosylated Chondroitin Sulfate (LFCS) from Sea Cucumber Cucumaria frondosa

机译:海参黄瓜低分子量岩藻糖基硫酸软骨素(LFCS)的体内抗癌机制

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摘要

The low-molecular-weight fucosylated chondroitin sulfate (LFCS) was prepared from native fucosylated chondroitin sulfate (FCS), which was extracted and isolated from sea cucumber Cucumaria frondosa, and the anti-cancer mechanism of LFCS on mouse Lewis lung carcinoma (LLC) was investigated. The results showed that LFCS remarkably inhibited LLC growth and metastasis in a dose-dependent manner. LFCS induced cell cycle arrest by increasing p53/p21 expression and apoptosis through activation of caspase-3 activity in LLC cells. Meanwhile, LFCS suppressed the expression of vascular endothelial growth factor (VEGF), increased the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) and downregulated the matrix metalloproteinases (MMPs) level. Furthermore, LFCS significantly suppressed the activation of ERK1/2/p38 MAPK/NF-κB pathway, which played a prime role in expression of MMPs. All of these data indicate LFCS may be used as anti-cancer drug candidates and deserve further study.
机译:低分子岩藻糖化硫酸软骨素(LFCS)是从海参黄瓜中提取并分离得到的天然岩藻糖化硫酸软骨素(FCS)制备的,其对小鼠路易斯肺癌(LLC)具有抗癌作用。被调查了。结果表明,LFCS以剂量依赖的方式显着抑制LLC的生长和转移。 LFCS通过激活LLC细胞中的caspase-3活性来增加p53 / p21表达和凋亡,从而诱导细胞周期停滞。同时,LFCS抑制血管内皮生长因子(VEGF)的表达,增加金属蛋白酶-1(TIMP-1)的组织抑制剂的表达,并下调基质金属蛋白酶(MMPs)的水平。此外,LFCS显着抑制ERK1 / 2 / p38 MAPK /NF-κB途径的激活,这在MMPs表达中起主要作用。所有这些数据表明LFCS可以用作抗癌药物候选者,值得进一步研究。

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