Elaidic Acid, a &lt;b&gt;&lt;i&gt;Trans&lt;/i&gt;&lt;/b&gt;-Fatty Acid, Enhances the Metastasis of Colorectal Cancer Cells

Ohmori, Hitoshi; Fujii, Kenichi; Kadochi, Yui; Mori, Shiori; Nishiguchi, Yukiko; Fujiwara, Rina; Kishi, Satoru; Sasaki, Takuma; Kuniyasu, Hiroki

doi:10.1159/000449205

Cited by 43 publications

(33 citation statements)

References 34 publications

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“…LA induces senescence in cultured CRC cells and dormancy in CRC cells inoculated into mice (11). Conversely, EA increases the proliferation of cells in spheres via the activation of epidermal growth factor receptor and the Wnt signaling pathway, and the upregulation of stem cell markers (16,17). EA also induces epithelial-mesenchymal transition and enhances tumor growth and metastasis (16,17).…”

Section: Discussionmentioning

confidence: 99%

Fatty acids inhibit anticancer effects of 5-fluorouracil in mouse cancer cell lines

et al. 2017

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The present study investigated the effects of two major dietary fatty acid components, linoleic acid (LA) and elaidic acid (EA), on the antitumor effects of 5-fluorouracil (5-FU) in the LL2, CT26 and CMT93 mouse cancer cell lines. Concurrent treatment with LA and 5-FU elicited a decreased cell viability compared with treatment with 5-FU alone. In addition, increased inhibition of growth was observed following concurrent treatment with EA and 5-FU. Sequential treatment of LA followed by 5-FU abrogated the anticancer effects of 5-FU, and treatment with EA followed by 5-FU increased cancer cell growth in addition to abrogating the anticancer effects of 5-FU. The expression of the stem cell markers CD133 and nucleostemin (NS) increased in all three cell lines treated concurrently with 5-FU and either LA or EA when compared with cells treated with 5-FU alone. Aldehyde dehydrogenase activity in the cancer stem cells (CSCs), in response to concurrent treatment with 5-FU and either LA or EA, was increased compared with 5-FU treatment alone. 5-FU inhibited the growth of CT26 tumors, but co-treatment with either LA or EA abrogated this effect. NS-positive CSCs were more abundant in CT26 tumors treated with 5-FU and either LA or EA compared with those treated with 5-FU alone. The results of the present study suggested that, rather than altering the sensitivity of cancer cells to 5-FU, LA and EA may promote the survival of CSCs. The results indicated that dietary composition during chemotherapy is an important issue.

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Section: Discussionmentioning

confidence: 99%

Fatty acids inhibit anticancer effects of 5-fluorouracil in mouse cancer cell lines

et al. 2017

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“…The cells (1x10 4 per well) were seeded in a 12-well dish. Cell growth was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay or by counting the number of cells with an Autocytometer (Sysmex, Kobe, Japan) after 48 h, as described previously (13 For analyzing the metastasis to the liver, lung, and peritoneum, cancer cells (1x10 6 cells) were inoculated into the spleen, the tail vein, or peritoneal cavity, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…We have previously reported the pro-tumoral effects of elaidic acid (EA), a major trans fatty acid (TFA) (4,5). EA is a long-chain fatty acid (LCFA) containing 18 carbon chains in a trans configuration, and is a structural isomer of oleic acid (OA).…”

Section: Introductionmentioning

confidence: 99%

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Pro‑metastatic signaling of the trans fatty acid elaidic acid is associated with lipid rafts

et al. 2018

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Abstract. Trans fatty acids (TFAs) are risk factors for cardiovascular disorders, and the cancer-promoting effects of TFAs have been previously reported. The present study examined the effects and signaling of elaidic acid (EA), a TFA, in colorectal cancer (CRC) cells. Oral intake of EA was found to increase metastasis of HT29 human CRC cells. Results indicated that, in the plasma membrane, EA was integrated into cholesterol rafts, which contain epidermal growth factor receptors (EGFR). EA increased nanog and c-myc, and decreased PGC-1A through lipid raft-associated EGFR signaling in HT29 cells. Depletion of cholesterol by methyl-β-cyclodextrin treatment abrogated the EA-induced stemness and oxidative phosphorylation. Simvastatin treatment also abrogated EA-enhanced tumor growth. These results indicate that EA enhances the stemness by activating EGFR in lipid rafts.

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“…TFA are associated with carcinogenesis [18][19][20] . Moreover, cancer metastasis [21,22] and drug resistance [23] are promoted by elaidic acid (EA), a major component of dietary TFA [24] , through the enhancement of stemness and epithelial-mesenchymal transition [22,23] .…”

Section: Introductionmentioning

confidence: 99%

Fatty Acids Induce Stemness in the Stromal Cells of a CT26 Mouse Tumor Model

Kawahara

Mori²,

Goto³

et al. 2017

Pathobiology

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The potential effects of 2 types of fatty acids on colorectal cancer (CRC) were assessed using cancer stromal cells. Linoleic acid (LA; C-18, n-6 unsaturated fatty acid) and elaidic acid (EA; C-18, trans acid), both known to affect colon carcinogenesis and cancer progression, were administered by gavage to BALB/c mice, which were inoculated with CT26 syngeneic colon cancer cells in the back. Both EA and LA treatments enhanced tumor growth and metastasis. EA and LA also increased the number of CD133-positive stromal cells in the tumor capsule. Importantly, those cancer cells at the tumor periphery, physically attached to CD133-positive stromal cells, also expressed CD133. These findings suggest that EA and LA might induce stemness in cancer cells through physical association and promote cancer metastasis.

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Elaidic Acid, a <b><i>Trans</i></b>-Fatty Acid, Enhances the Metastasis of Colorectal Cancer Cells

Cited by 43 publications

References 34 publications

Fatty acids inhibit anticancer effects of 5-fluorouracil in mouse cancer cell lines

Fatty acids inhibit anticancer effects of 5-fluorouracil in mouse cancer cell lines

Pro‑metastatic signaling of the trans fatty acid elaidic acid is associated with lipid rafts

Fatty Acids Induce Stemness in the Stromal Cells of a CT26 Mouse Tumor Model

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