Fam Cancer, 2015, Volume 14; Issue 1: Pages 25 - 30

Down-regulation of malignant potential by alpha linolenic acid in human and mouse colon cancer calls

Chamberland, JP. Moon, H-S.

Key Findings:

In models of colon cancer, ALA reduced malignant potential (cell adhesion, invasion and colony formation) and also decreased tumor cell growth and colony size. The disruption of cell adhesion and colony formation can reduce the ability of the cancer cells to metastasize. The authors suggest that therapies that target metastasis may be able to assist in the survival of cancer patients.

ABSTRACT:

This study examines the role that ALA may play in reducing colon cancer. ALA reduced metastasis (the ability of the cancer cell to travel) and the ability of the cancer cells to adhere to tissues. ALA reduced the size of carcinogenic colonies in human and mouse colon cell lines. The results showed that ALA directly controls the malignant potential of human and mouse colon cancer cell lines. Further clinical work is suggested following the positive results of this mechanistic study. Abstract: Omega 3 fatty acids (also called n3 fatty acid) are polyunsaturated fatty acids (PUFAs) with a double bond (C =C) at the third carbon atom from the end of the carbon chain. Numerous test tube and animal studies have shown that omega3 fatty acids may prevent or inhibit the growth of cancers, suggesting that omega3 fatty acids are important in cancer physiology. Alpha linolenic acid (ALA) is one of an essential omega 3 fatty acid and organic compound found in seeds (chia and flaxseed), nuts (notably walnuts), and many common vegetable oils. ALA has also been shown to down regulate cell proliferation of prostate, breast, and bladder cancer cells. However, direct evidence that ALA suppresses to the development of colon cancer has not been studied. Also, no previous studies have evaluated whether ALA may regulate malignant potential (adhesion, invasion and colony formation) in colon cancer cells. In order to address the questions above, we conducted in vitro studies and evaluated whether ALA may downregulate malignant potential in human (HT29 and HCT116) and mouse (MCA38) colon cancer cell lines. We observed that treatment with 1 to 5 mm of ALA inhibits cell proliferation, adhesion and invasion in both human and mouse colon cancer cell lines. Interestingly, we observed that ALA did not decrease total colony numbers when compared to control. By contrast, we found that size of colony was significantly changed by ALA treatment when compared to control in all colon cancer cell lines. We suggest that our data enhance our current knowledge of ALA’s mechanism and provide crucial information to further the development of new therapies for the management or chemoprevention of colon cancer. (Authors Abstract)

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