High oleic acid oil suppresses lung tumorigenesis in mice through the modulation of extracellular signal-regulated kinase cascade |
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Authors: | Yamaki Tatsuya Yano Tomohiro Satoh Haruna Endo Tatsuo Matsuyama Chinami Kumagai Hitomi Miyahara Mitsuyoshi Sakurai Hidetoshi Pokorny Jan Shin Sung Jae Hagiwara Kiyokazu |
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Affiliation: | (1) College of Bioresource Sciences, Nihon University, Fujisawa, 252-8510 Kanagawa, Japan;(2) Faculty of Food and Biochemical Technology, Institute of Chemical Technology, CZ-16628 Prague 6, Czech Republic;(3) Department of Food Science Research for Health, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, 162-8636 Tokyo, Japan |
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Abstract: | This study was undertaken to estimate the effect of dietary high oleic acid oil (OA) on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
(NNK)-induced lung tumorigenesis in mice. Diet containing 10% oil was fed to mice through experimental periods. On day 30
after NNK injection (100 mg/kg body weight, i.p.), the treatment increased the level of prostaglandin E2 (PGE2) as well as proliferating cell nuclear antigen, a marker of cell proliferation in a high linoleic acid oil (LA)-fed group
but not in an OA-fed group. The NNK treatment also induced the activation of an extracellular signal-regulated kinase (Erk)
cascade (Erk, Mek and Raf-1) in an LA-fed group. On the other hand, OA feeding abolished the NNK-induced activation of the
Erk cascade. In conjugation with these events, OA feeding reduced lung tumor incidence and tumor multiplicity (percentage
of mice with tumors) in mice compared with LA feeding at the 20th experimental week. These results suggest that OA suppresses
lung tumorigenesis and that this suppression is correlated with the inhibition of PGE2 production and inactivation of the Erk cascade. |
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