PT  - JOURNAL ARTICLE
AU  - TERASAKI, MASARU
AU  - INOUE, TAKUYA
AU  - MURASE, WATARU
AU  - KUBOTA, ATSUHITO
AU  - KOJIMA, HIROYUKI
AU  - KOJOMA, MARESHIGE
AU  - OHTA, TOHRU
AU  - MAEDA, HAYATO
AU  - MIYASHITA, KAZUO
AU  - MUTOH, MICHIHIRO
AU  - TAKAHASHI, MAMI
TI  - Fucoxanthinol Induces Apoptosis in a Pancreatic Intraepithelial Neoplasia Cell Line
AID  - 10.21873/cgp.20248
DP  - 2021 Mar 01
TA  - Cancer Genomics - Proteomics
PG  - 133--146
VI  - 18
IP  - 2
4099  - http://cgp.iiarjournals.org/content/18/2/133.short
4100  - http://cgp.iiarjournals.org/content/18/2/133.full
SO  - Cancer Genomics Proteomics2021 Mar 01; 18
AB  - 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 Ptf1aCre/+; LSL-k-rasG12D/+ 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.