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A fish oil/pectin diet beneficially altered gene profiles during radiation‐enhanced colon carcinogenesis
Author(s) -
Kim Hyemee,
Turner Nancy D,
Taddeo Stella S,
Davidson Laurie A,
Wang Naisyin,
Vannucci Marina,
Chapkin Robert S,
Carroll Raymond J,
Lupton Joanne R
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.885.9
Subject(s) - autophagy , fish oil , apoptosis , carcinogenesis , mapk/erk pathway , carcinogen , chemistry , corn oil , cell growth , cancer research , endocrinology , biology , medicine , signal transduction , gene , fish <actinopterygii> , biochemistry , fishery
The goal of this project was to determine the effect of diet on the patterns of gene expression in exfoliated colonocytes from rats exposed to radiation (+/− 1 Gy, 1 GeV/nucleon Fe ions) and a chemical carcinogen (AOM, 2x, 15 mg/kg BW). Rats received corn oil/cellulose (CC) or fish oil/pectin (FP) diets for 3 wk prior to radiation exposure, which was followed by AOM injections 10 and 17 d later. Isolated poly A+ RNA from exfoliated colonocytes was analyzed using GE Codelink arrays. The radiation and diet interaction resulted in differences in expression of 95 genes, including five genes involved in the MAPK signaling pathway and regulation of autophagy. For example, irradiated rats consuming FP had ∼1.7 times the level of Ppm1b, a MAPK signaling suppressor, found in CC rats (P=0.036), suggesting the FP diet would suppress cell proliferation in rats exposed to radiation. With respect to autophagy, the expression of Atg7 in non‐irradiated rats consuming FP was higher than the level in CC rats (P=0.003), suggesting the FP rats would likely have elevated apoptosis via autophagy. FP may suppress cell proliferation and enhance autophagy in the colon and thereby suppress colon carcinogenesis caused by radiation and AOM. Supported by NSBRI (NASA NCC 9‐58), NIH (CA57030 and CA59034) and NIEHS (P30‐ES09106).