1. Effect of Fucoxanthinol on Pancreatic Ductal Adenocarcinoma Cells from an N-Nitrosobis(2-oxopropyl)amine-initiated Syrian Golden Hamster Pancreatic Carcinogenesis Model
- Author
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Michihiro Mutoh, Masaru Terasaki, Takuji Tanaka, Yusaku Nishizaka, Wataru Murase, Hayato Maeda, Kazuo Miyashita, Mami Takahashi, Hiroyuki Kojima, Atsuhito Kubota, and Mareshige Kojoma
- Subjects
Cancer Research ,Carcinogenesis ,Hamster ,Adenocarcinoma ,Biochemistry ,Pancreatic cancer ,Cricetinae ,Genetics ,medicine ,Animals ,Humans ,Anoikis ,Molecular Biology ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Chemistry ,Cancer ,Cell cycle ,medicine.disease ,beta Carotene ,Disease Models, Animal ,Apoptosis ,Cancer research ,Female ,Research Article ,Carcinoma, Pancreatic Ductal - Abstract
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. Materials and methods FxOH action and its molecular mechanisms were investigated in HaPC cells using flow-cytometry, comprehensive gene array, and western blotting analyses. Results 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. Conclusion FxOH may have a high potential as a cancer chemopreventive agent in a hamster pancreatic carcinogenesis model.
- Published
- 2021