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岩藻聚糖诱导 HT-29 人结肠癌细胞凋亡及其对 ErbB 信号的调控。

Induction of apoptosis and the regulation of ErbB signaling by laminarin in HT-29 human colon cancer cells.

机构信息

Department of Food and Life Science, Pukyong National University, Nam-gu, Busan 608-737, Republic of Korea.

出版信息

Int J Mol Med. 2013 Aug;32(2):291-5. doi: 10.3892/ijmm.2013.1409. Epub 2013 Jun 5.

DOI:10.3892/ijmm.2013.1409
PMID:23739740
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3776715/
Abstract

Laminarin, found in marine brown algae, is used as a carbohydrate reserve for phytoplankton; however, it is also used in traditional Chinese medicine, and has been shown to have several biological activities, including anticancer activities. In this study, we examined the mechanisms through which laminarin from Laminaria digitata induces apoptosis in HT-29 colon cancer cells, as well as the involvement of the ErbB signaling pathway. Cell viability assay revealed that laminarin induced cell death in a dose-dependent manner. Cell cycle analysis revealed that laminarin increased the percentage of cells in the sub-G1 and G2-M phase. Western blot analysis demonstrated that laminarin inhibited the heregulin-stimulated phosphorylation of ErbB2. A decrease in cellular proliferation was also observed; this was found to be dependent on ErbB, which activates c-Jun N-terminal kinase. These findings demonstrate the important role of the epidermal growth factor receptor in colon cancer tumorigenesis, and suggest the potential of laminarin as a bio-functional food with anticancer effects on human colon cancer.

摘要

昆布多糖,存在于海洋褐藻中,被用作浮游植物的碳水化合物储备;然而,它也被用于传统中药,并已被证明具有多种生物活性,包括抗癌活性。在这项研究中,我们研究了来自海带的昆布多糖诱导 HT-29 结肠癌细胞凋亡的机制,以及 ErbB 信号通路的参与。细胞活力测定显示,昆布多糖以剂量依赖的方式诱导细胞死亡。细胞周期分析显示,昆布多糖增加了处于 sub-G1 和 G2-M 期的细胞百分比。Western blot 分析表明,昆布多糖抑制了 HERE 刺激的 ErbB2 磷酸化。还观察到细胞增殖减少;这被发现依赖于激活 c-Jun N-末端激酶的表皮生长因子受体。这些发现表明,表皮生长因子受体在结肠癌肿瘤发生中起着重要作用,并表明昆布多糖作为一种具有抗癌作用的功能性食品,对人类结肠癌具有潜在的应用价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/4fc4ab54a60c/IJMM-32-02-0291-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/8ca3a096db24/IJMM-32-02-0291-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/2156853d4162/IJMM-32-02-0291-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/e4c0de13ea57/IJMM-32-02-0291-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/d1787bf6b584/IJMM-32-02-0291-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/4fc4ab54a60c/IJMM-32-02-0291-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/8ca3a096db24/IJMM-32-02-0291-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/2156853d4162/IJMM-32-02-0291-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/e4c0de13ea57/IJMM-32-02-0291-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/d1787bf6b584/IJMM-32-02-0291-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df9c/3776715/4fc4ab54a60c/IJMM-32-02-0291-g04.jpg

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