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Trans fats increase proliferation and membrane complexity in A549 human lung carcinoma cells
Author(s) -
BushO'Donnell Jennifer,
Siddiqui Rafat,
Stillwell William
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb42-c
Subject(s) - polyunsaturated fatty acid , apoptosis , lung cancer , elaidic acid , chemistry , a549 cell , biochemistry , linoleic acid , medicine , fatty acid
The varied health benefits of polyunsaturated fatty acids (PUFA) are well‐documented and include prevention of cardiovascular disease and cancer. These beneficial lipids are typically long chain PUFA in the cis conformation, especially those of the omega‐3 class. Conversely those with a trans configuration, “trans fats,” have been implicated as a significant factor in heart disease. However, little is known about their relation to cancer. This study seeks to ascertain the effects of trans fats in comparison to cis‐PUFA on lung carcinoma in vitro. It was shown that incubation of A549 human lung carcinoma cells with trans fats such as elaidic acid (EA, 18:1, n‐9) increased proliferation and membrane complexity as compared to incubation with cis‐lipids, several of which including docosohexaenoic acid (DHA, 22:6, n‐3) and linolenic acid (LLA, 18:3, n‐6) decreased proliferation. Caspase‐3 activation, a late step in the apoptosis pathway, was accordingly higher in cells treated with cis‐PUFA as compared to the untreated control. Those treated with trans fats showed a reduction in caspase‐3. Chemotaxis was reduced by nearly all the tested cis‐ and trans‐PUFA, while each lipid increased adhesion. Marked increases in adhesion were irrelevant of conformation, with petroselenic acid (PSA, 18:1, n‐6), (cis), transvassenic acid (TVA, 18:1, n‐11) and linoelaidic acid (LEA, 18:2, n‐9, 11) (both trans) showing the greatest increase. This work suggests that trans fats may have a complex role in some aspects of cancer proliferation, while any role in cell migration and adhesion remain questionable. The in vitro work outlined here provides a basis for further in vivo investigation. Supported by NIH