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Establishing the anti-cancer effects of unsaturated fatty acids and a novel oil on human breast cancer cells Open Access


Other title
cell membrane
n-3 fatty acids
unsaturated fatty acids
breast cancer
conjugated linoleic acid
n-6 fatty acids
Type of item
Degree grantor
University of Alberta
Author or creator
Yu, Howe-Ming
Supervisor and department
Field, Catherine (AFNS)
Examining committee member and department
Mazurak, Vera (AFNS)
Weselake, Randall (AFNS)
Department of Agricultural, Food, and Nutritional Science
Nutrition & Metabolism
Date accepted
Graduation date
Master of Science
Degree level
N-3 and n-6 fatty acids and conjugated linoleic (CLA) acid have been known to inhibit breast cancer cell growth, however, effects on normal cells and of single and mixtures of n-3 and n-6 pathway intermediates have not been thoroughly investigated. The objective of this thesis was to determine the effects of fatty acids with potential anti-cancer activity and a fatty acid mixture, representing a new plant source, on breast cell viability and cell membrane composition. Human tumorigenic MDA-MB-231 and MCF-7 cells lines and a non-tumorigenic MCF-12A cell line were studied. All fatty acids, including the mixture representing a stearidonic acid (SDA) enriched flax oil (SO) reduced the viability of tumorigenic but not non-tumorigenic cells, compared to cells without fatty acids (p<0.05). α-linolenic acid, docosahexaenoic acid (DHA), linoleic acid, and arachidonic acid (AA) from treatments were minimally converted down their respective pathways and incorporated into membranes as the original fatty acid. Intermediates SDA, eicosatetraenoic acid and eicosapentaenoic acid showed significant conversion down the n-3 pathway, but not to DHA. N-6 γ-linolenic acid and dihomo-γ-linolenic acid (DGLA) treatments accumulated DGLA in the phospholipids, but not AA. SO treatment showed conversion to docosapentaenoic acid and DGLA in tumorigenic cell lines, but was not well converted in MCF-12A cells. C9, t11-CLA decreased tumorigenic growth (p<0.05) and was isomerized to a more potent isomer on cell viability. Overall, our data demonstrates that in vitro, n-3 and n-6 fatty acid intermediates, CLA and a n-3 and n-6 mixture decrease tumorigenic cell viability and are incorporated into membranes with significant conversion down their pathways. Inhibitory effects of n-3 and n-6 fatty acid intermediates seem to be independent of conversion to biological endpoints, and c9, t11-CLA’s inhibitory effects may be due to its isomerization.
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