Abstract | OBJECTIVES: METHODS: The effects of EPA on proliferation of three human pancreatic cancer cell lines (SW1990, AsPC-1, and PANC-1) were assessed. Induction of apoptosis and expressions of apoptosis-related proteins were measured. The effect of EPA on cyclo-oxygenase-2 expression in these cell lines was determined. RESULTS: EPA inhibited proliferation of all three human pancreatic cancer cell lines in a dose-dependent fashion. Simultaneously, EPA treatment induced apoptosis and this was associated with caspase-3 activation. EPA treatment was also associated with a decrease in intracellular levels of cyclo-oxygenase-2 protein. CONCLUSION: We have demonstrated that EPA inhibits human pancreatic cancer cell growth due at least in part to the induction of apoptotic cell death. Such apoptosis is associated with activation of caspase-3 and suppression of cyclo-oxygenase-2 expression. Greater understanding of the molecular events associated with the biological activity of EPA should enhance the therapeutic potential of administration of EPA to patients who have pancreatic cancer.
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Authors | Tetsuya Shirota, Seiji Haji, Mitsuo Yamasaki, Takuya Iwasaki, Toshiharu Hidaka, Yoshifumi Takeyama, Hitoshi Shiozaki, Harumasa Ohyanagi |
Journal | Nutrition (Burbank, Los Angeles County, Calif.)
(Nutrition)
Vol. 21
Issue 10
Pg. 1010-7
(Oct 2005)
ISSN: 0899-9007 [Print] United States |
PMID | 16157238
(Publication Type: Journal Article)
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Chemical References |
- Cyclooxygenase 2 Inhibitors
- Eicosapentaenoic Acid
- Cyclooxygenase 2
- CASP3 protein, human
- Caspase 3
- Caspases
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Topics |
- Apoptosis
(drug effects)
- Caspase 3
- Caspases
(metabolism)
- Cell Division
(drug effects)
- Cell Line, Tumor
- Cyclooxygenase 2
(drug effects, metabolism)
- Cyclooxygenase 2 Inhibitors
(pharmacology)
- Dose-Response Relationship, Drug
- Eicosapentaenoic Acid
(pharmacology)
- Humans
- Pancreatic Neoplasms
(drug therapy, pathology, ultrastructure)
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