AIM: To investigate the impact of arachidonic acid (AA) and docosahexaenoic acid (DHA) and their combination on colon cancer cell growth. METHODS: The LS-174T colon cancer cell line was used to study the role of the prostaglandin precursor AA and the omega-3 polyunsaturated fatty acid DHA on cell growth. Cell viability was assessed in XTT assays. For analysis of cell cycle and cell death, flow cytometry and DAPI staining were applied. Expression of cyclooxygenase-2 (COX-2), p21 and bcl-2 in cells incubated with AA or DHA was examined by real-time RT-PCR. Prostaglandin E(2) (PGE(2)) generation in the presence of AA and DHA was measured using a PGE(2)-ELISA. RESULTS: AA increased cell growth, whereas DHA reduced viability of LS 174T cells in a time- and dose-dependent manner. Furthermore, DHA down- regulated mRNA of bcl-2 and up-regulated p21. Interestingly, DHA was able to suppress AA-induced cell proliferation and significantly lowered AA-derived PGE(2) formation. DHA also down-regulated COX-2 expression. In addition to the effect on PGE(2) formation, DHA directly reduced PGE(2)-induced cell proliferation in a dose-dependent manner. CONCLUSION: These results suggest that DHA can inhibit the pro-proliferative effect of abundant AA or PGE(2).
AIM: To investigate the impact of arachidonic acid (AA) and docosahexaenoic acid (DHA) and their combination on colon cancer cell growth. METHODS: The LS-174T colon cancer cell line was used to study the role of the prostaglandin precursor AA and the omega-3 polyunsaturated fatty acidDHA on cell growth. Cell viability was assessed in XTT assays. For analysis of cell cycle and cell death, flow cytometry and DAPI staining were applied. Expression of cyclooxygenase-2 (COX-2), p21 and bcl-2 in cells incubated with AA or DHA was examined by real-time RT-PCR. Prostaglandin E(2) (PGE(2)) generation in the presence of AA and DHA was measured using a PGE(2)-ELISA. RESULTS: AA increased cell growth, whereas DHA reduced viability of LS 174T cells in a time- and dose-dependent manner. Furthermore, DHA down- regulated mRNA of bcl-2 and up-regulated p21. Interestingly, DHA was able to suppress AA-induced cell proliferation and significantly lowered AA-derived PGE(2) formation. DHA also down-regulated COX-2 expression. In addition to the effect on PGE(2) formation, DHA directly reduced PGE(2)-induced cell proliferation in a dose-dependent manner. CONCLUSION: These results suggest that DHA can inhibit the pro-proliferative effect of abundant AA or PGE(2).
Authors: Wangsheng Yu; Nicole R Murray; Capella Weems; Lu Chen; Huiping Guo; Richard Ethridge; Jeffrey D Ceci; B Mark Evers; E Aubrey Thompson; Alan P Fields Journal: J Biol Chem Date: 2002-12-11 Impact factor: 5.157
Authors: Yvonne E M Dommels; Merel M G Haring; Nynke G M Keestra; Gerrit M Alink; Peter J van Bladeren; Ben van Ommen Journal: Carcinogenesis Date: 2003-03 Impact factor: 4.944
Authors: E D Courtney; S Matthews; C Finlayson; D Di Pierro; A Belluzzi; E Roda; J Y Kang; R J Leicester Journal: Int J Colorectal Dis Date: 2007-01-10 Impact factor: 2.796