Down-regulation of malignant potential by alpha linolenic acid in human and mouse colon cancer cells
Down-regulation of malignant potential by alpha linolenic acid in human and mouse colon cancer cells
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DOI：
10.1007/s10689-014-9762-z
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发表时间：
2015-03-01
期刊：
影响因子：
2.2
通讯作者：
Moon, Hyun-Seuk
中科院分区：
文献类型：
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作者：
Chamberland, John P.;Moon, Hyun-Seuk
ω-3脂肪酸（也称为ω-3脂肪酸或n-3脂肪酸）是在碳链末端的第三个碳原子处具有双键（C=C）的多不饱和脂肪酸（PUFA）。许多试管和动物研究表明，omega-3脂肪酸可以预防或抑制癌症的生长，这表明omega-3脂肪酸在癌症生理学中很重要。α-亚麻酸（ALA）是一种必需的ω-3脂肪酸和有机化合物，存在于种子（奇亚和亚麻籽），坚果（特别是核桃）和许多常见的植物油中。ALA还被证明可以下调前列腺癌、乳腺癌和膀胱癌细胞的细胞增殖。然而，ALA抑制结肠癌发展的直接证据尚未研究。此外，以前没有研究评估ALA是否可以调节结肠癌细胞的恶性潜能（粘附，侵袭和集落形成）。为了解决上述问题，我们进行了体外研究，并评估了ALA是否可以下调人（HT 29和HCT 116）和小鼠（MCA 38）结肠癌细胞系的恶性潜能。我们观察到用1-5 mM ALA处理抑制人和小鼠结肠癌细胞系中的细胞增殖、粘附和侵袭。有趣的是，我们观察到ALA与对照相比没有减少总菌落数。相比之下，我们发现在所有结肠癌细胞系中，与对照相比，ALA处理显著改变了集落的大小。我们认为，我们的数据增强了我们目前对ALA机制的了解，并为进一步开发用于结肠癌管理或化学预防的新疗法提供了重要信息。
Omega-3 fatty acids (also called omega-3 fatty acis or n-3 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 omega-3 fatty acids may prevent or inhibit the growth of cancers, suggesting that omega-3 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 down-regulate malignant potential in human (HT29 and HCT116) and mouse (MCA38) colon cancer cell lines. We observed that treatment with 1-5 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.