岩藻黄质醇诱导胰腺上皮内瘤变细胞凋亡。
A Fucoxanthinol Induces Apoptosis in a Pancreatic Intraepithelial Neoplasia Cell.
作者信息
Terasaki Masaru, Inoue Takuya, Murase Wataru, Kubota Atsuhito, Kojima Hiroyuki, Kojoma Mareshige, Ohta Tohru, Maeda Hayato, Miyashita Kazuo, Mutoh Michihiro, Takahashi Mami
机构信息
School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Hokkaido, Japan;
Advanced Research Promotion Center, Health Sciences University of Hokkaido, Hokkaido, Japan.
出版信息
Cancer Genomics Proteomics. 2021 Mar-Apr;18(2):133-146. doi: 10.21873/cgp.20248.
BACKGROUND/AIM: Fucoxanthinol (FxOH), a predominant metabolite from fucoxanthin (Fx), can exert potential anti-cancer effects in various cancers. However, limited data are available on the effect of FxOH or Fx on pancreatic cancer. The present study investigated the effect of FxOH on a cell line derived from pancreatic cancer tissue developed in Ptf1a; LSL-k-ras mice.
MATERIALS AND METHODS
Using flow-cytometric, microarrays, and western blotting analyses, alterations in FxOH-induced apoptosis-related gene expression and protein levels were evaluated in a mice pancreatic cancer cell line, KMPC44.
RESULTS
FxOH significantly arrested the cells at S phase along with suppression of many gene sets, such as cytokine- cytokine receptor interaction and cell adhesion molecule CAMS. Moreover, attenuated protein levels for cytokine receptors, adhesion, phosphatidylinositol-3 kinase/protein kinase B, and mitogen-activated protein kinase were observed.
CONCLUSION
FxOH may prevent pancreatic cancer development in a murine cancer model.
背景/目的：岩藻黄质醇（FxOH）是岩藻黄质（Fx）的主要代谢产物，可在多种癌症中发挥潜在的抗癌作用。然而，关于FxOH或Fx对胰腺癌作用的数据有限。本研究调查了FxOH对源自Ptf1a；LSL-k-ras小鼠所患胰腺癌组织的细胞系的影响。
材料与方法
使用流式细胞术、微阵列和蛋白质印迹分析，在小鼠胰腺癌细胞系KMPC44中评估FxOH诱导的凋亡相关基因表达和蛋白质水平的变化。
结果
FxOH使细胞显著停滞于S期，同时抑制了许多基因集，如细胞因子-细胞因子受体相互作用和细胞黏附分子（CAMS）。此外，观察到细胞因子受体、黏附、磷脂酰肌醇-3激酶/蛋白激酶B和丝裂原活化蛋白激酶的蛋白质水平降低。
结论
FxOH可能在小鼠癌症模型中预防胰腺癌的发展。
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