Trans fatty acid elaidic acid makes colorectal cancer more aggressive

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Ohmori H. at Nara Medical University in Kashihara, Japan and colleagues published a study in 2017 to indicate trans fat (olaidic acid) increases the metastasis of colorectal cancer.

The study in Pathobiology showed elaidic acid (a trans fatty acid) enhanced the growth, survival and invasion of the colorectal cell lines CT26 and HT29.

Compared to the treatment with oleic acid – a natural cis isomer of elaidic acid or control, treatment with the trans fatty acid more significantly enhanced tumor growth and metastasis of the colorectal cancer cells in the lung, liver and peritoneum.

When treated with elaidic acid and in comparison with oleic acid, more colorectal cancer cells formed spheres. And elaidic acid treatment led to the expression of the stemness factors like nucleostemin, CD133 and Oct4, compared to oleic acid treatment.

In addition, treatment with elaidic acid led to the formation of larger spheres of colorectal cancer cells, compared to the oleic acid treatment.

Oral intake of elaidic acid also boosted liver metastasis and CD133 expression of colorectal cancer cells in a dose-responsive manner. That is, high intake of the trans fatty acid caused high expression of CD133 and increased the stemness of the cancer cells.

Elaidic acid also interferes with a chemotherapy drug called 5-fluorouracil, specifically increasing the drug resistance of the cancer cells to the chemotherapy.

The authors concluded “Our findings demonstrate that EA might provide prominent metastatic potential to CRC cells (colorectal cancer cells), which shows important implications for the treatment of CRC.”

Elaidic acid is the major form of trans fat found in hydrogenated vegetable oils and it is the trans isomer of oleic acid.

The message is clear that patients should use a diet free of trans fat to help colorectal cancer treatment. This study may also suggest that trans fat could potentially interfere with the treatment of other types of cancers. (Dr. Lu)

Pathobiology 2017;84:144-151, https://doi.org/10.1159/000449205

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