School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Hokkaido, Japan;
Advanced Research Promotion Center, Health Sciences University of Hokkaido, Hokkaido, Japan.
Cancer Genomics Proteomics. 2021 May-Jun;18(3 Suppl):407-423. doi: 10.21873/cgp.20268.
BACKGROUND/AIM: Fucoxanthinol (FxOH) is a marine carotenoid metabolite with potent anti-cancer activity. However, little is known about the efficacy of FxOH in pancreatic cancer. In the present study, we investigated the inhibitory effect of FxOH on six types of cells cloned from N-nitrosobis(2-oxopropyl)amine (BOP)-induced hamster pancreatic cancer (HaPC) cells.
FxOH action and its molecular mechanisms were investigated in HaPC cells using flow-cytometry, comprehensive gene array, and western blotting analyses.
FxOH (5.0 μM) significantly suppressed the growth of four out of six types of HaPC cells. Moreover, FxOH significantly suppressed cell cycle, chemokine, integrin, actin polymerization, microtubule organization and PI3K/AKT and TGF-β signals, and activated caspase-3 followed by apoptosis and anoikis induction in HaPC-5 cells.
FxOH may have a high potential as a cancer chemopreventive agent in a hamster pancreatic carcinogenesis model.
背景/目的:岩藻黄质醇(FxOH)是一种具有强大抗癌活性的海洋类胡萝卜素代谢物。然而,关于 FxOH 在胰腺癌中的疗效知之甚少。在本研究中,我们研究了 FxOH 对 N-亚硝基双(2-氧丙基)胺(BOP)诱导的仓鼠胰腺癌(HaPC)细胞克隆的六种细胞的抑制作用。
使用流式细胞术、综合基因阵列和 Western blot 分析研究了 FxOH 在 HaPC 细胞中的作用及其分子机制。
FxOH(5.0 μM)显著抑制了六种 HaPC 细胞中的四种细胞的生长。此外,FxOH 显著抑制了细胞周期、趋化因子、整合素、肌动蛋白聚合、微管组织和 PI3K/AKT 和 TGF-β 信号,并激活了 caspase-3,随后诱导 HaPC-5 细胞凋亡和失巢凋亡。
FxOH 可能作为一种癌症化学预防剂在仓鼠胰腺癌发生模型中具有很高的潜力。