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Elaidic Acid, a <b><i>Trans</i></b>-Fatty Acid, Enhances the Metastasis of Colorectal Cancer Cells
Author(s) -
Hitoshi Ohmori,
Kiyomu Fujii,
Yui Kadochi,
Shiori Mori,
Yukiko Nishiguchi,
Rina Fujiwara,
Shingo Kishi,
Takamitsu Sasaki,
Hiroki Kuniyasu
Publication year - 2016
Publication title -
pathobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.941
H-Index - 53
eISSN - 1423-0291
pISSN - 1015-2008
DOI - 10.1159/000449205
Subject(s) - metastasis , cancer research , colorectal cancer , medicine , elaidic acid , cancer cell , cancer , chemistry , endocrinology , fatty acid , biochemistry , linoleic acid
The effects of trans-fatty acids (TFAs) on cardiovascular disorders have been extensively studied, and the effect of TFAs on cancers has recently been recognized. This study examined the effects of elaidic acid (EA), a TFA, on colorectal cancer (CRC) progression. We demonstrated that EA enhanced the growth, survival, and invasion of the CRC cell lines, CT26, and HT29. Tumor growth and metastasis in the lung, liver, and peritoneum were significantly more enhanced in CRC cells treated with EA than those treated with the cis form of EA, oleic acid (OA), or vehicle. Spheres of CRC cells were formed at more pronounced numbers in EA-treated cells than in OA-treated cells. Compared to OA, EA treatment also induced expression of the stemness factors, nucleostemin, CD133, and Oct4. Moreover, spheres of EA-treated CRC cells were larger and more proliferative than spheres of OA-treated cells. Oral intake of EA also enhanced liver metastasis and CD133 expression of CRC cells in a dose-dependent manner. EA intake also increased resistance to 5-fluorouracil. Inhibition of Wnt and ERK1/2 abrogated EA-induced enhancement of metastasis. Our findings demonstrate that EA might provide prominent metastatic potential to CRC cells, which shows important implications for the treatment of CRC.

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