2009 study posted for filing
Colon cancer is one of the leading causes of death in Western countries. The role of n-3 and n-6 PUFAs in colorectal carcinoma cell growth has not been well studied. It is known that PGE2, generated from AA, is an important factor in the tumorigenesis of colorectal cancer. However, previous in vitro observations have led to uncertainty regarding a differential role of n-3 and n-6 PUFA for growth of tumor cells, as some findings are contradictory, and most studies have not addressed the effect of a changed n-3/n-6 PUFA ratio on cell proliferation.
A research article to be published on March 7, 2009 in the World Journal of Gastroenterology addresses this question. The research team around Piet Habbel and Karsten H. Weylandt from the Charité University Hospital in Berlin (Germany) and led by Jing X. Kang from the Massachusetts General Hospital in Boston (USA) used the LS-174T colon cancer cell line, for which several previous studies have shown an important role of PGE2 as growth promoting agent. The study showed differential effects of n-6 PUFA AA and n-3 PUFA DHA. While proliferation was promoted by AA, incubation with DHA reduced cell growth and viability. In addition, this study demonstrated that the n-3 PUFA DHA can directly suppress AA- as well as PGE2-induced colon cancer cell growth.
These results add evidence to the argument that the ratio of n-6/n-3 PUFA (and in particular the ratio of AA versus DHA) may be a critical determinant of proliferation and tumor growth in the colon, and that DHA supplementation can suppress tumor cell growth, even in the presence of high AA- and PGE2 levels. These results suggest that supplementation of DHA may be a powerful tool to counteract AA- and PGE2-promoted colon cancer cell growth that is associated with the predominant Western diet.
Reference: Habbel P, Weylandt KH, Lichopoj K, Nowak J, Purschke M, Wang JD, He CW, Baumgart DC, Kang JX. Docosahexaenoic acid suppresses arachidonic acid-induced proliferation of LS-174T human colon carcinoma cells. World J Gastroenterol 2009; 15(9): 1079-1084
Correspondence to: Karsten H Weylandt, MD, PhD, Dr. Kang’s Lab, Massachusetts General Hospital, 149-13th Street, Room 4433, Charlestown, MA 02129,United States. email@example.com
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