Premium
High oleic acid oil suppresses lung tumorigenesis in mice through the modulation of extracellular signal‐regulated kinase cascade
Author(s) -
Yamaki Tatsuya,
Yano Tomohiro,
Satoh Haruna,
Endo Tatsuo,
Matsuyama Chinami,
Kumagai Hitomi,
Miyahara Mitsuyoshi,
Sakurai Hidetoshi,
Pokorny Jan,
Shin Sung Jae,
Hagiwara Kiyokazu
Publication year - 2002
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-002-0961-8
Subject(s) - mapk/erk pathway , carcinogenesis , extracellular , kinase , endocrinology , chemistry , prostaglandin e2 , medicine , cell growth , oleic acid , prostaglandin , clinical chemistry , cancer research , biochemistry , biology , gene
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 E 2 (PGE 2 ) 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 PGE 2 production and inactivation of the Erk cascade.