Back to Search
Start Over
Growth inhibition and apoptosis induction by all-trans-conjugated linolenic acids on human colon cancer cells.
- Source :
-
Anticancer research [Anticancer Res] 2006 May-Jun; Vol. 26 (3A), pp. 1855-60. - Publication Year :
- 2006
-
Abstract
- Conjugated linolenic acids (CLN) are geometric and positional isomers of linolenic acid. Growth inhibition and apoptosis induction by alpha-eleostearic acid (c9,t11,t13-CLN), beta-eleostearic acid (t9,t11,t13-CLN), alpha-calendic acid (t8,t10,c12-CLN) and beta-calendic acid (t8,t10,t12-CLN) were compared. beta-Eleostearic acid and beta-calendic acid, which have all-trans-conjugated double bonds, exerted stronger growth inhibition and more DNA fragmentation, an indicator of apoptosis induction, in the human colon cancer cells Caco-2 than alpha-eleostearic acid and alpha-calendic acid with the cis configuration. Down-regulation of bcl-2 and up-regulation of bax mRNA by beta-eleostearic acid were also greater than by alpha-eleostearic acid. Interestingly, the cytotoxic effects of beta-eleostearic acid and beta-calendic acid were not counteracted completely by alpha-tocopherol, whereas the cytotoxic effects of alpha-eleostearic and alpha-calendic acids were lost in the presence of alpha-tocopherol. These results suggest that beta-eleostearic and beta-calendic acids have signaling pathways different from those of alpha-eleostearic and alpha-calendic acids and exhibit high potency for reducing the cell viability of Caco-2.
- Subjects :
- Caco-2 Cells
Cell Growth Processes drug effects
Colonic Neoplasms pathology
Down-Regulation
Fatty Acids, Unsaturated pharmacology
Humans
Isomerism
Proto-Oncogene Proteins c-bcl-2 biosynthesis
Proto-Oncogene Proteins c-bcl-2 genetics
RNA, Messenger biosynthesis
RNA, Messenger genetics
Up-Regulation
alpha-Tocopherol pharmacology
bcl-2-Associated X Protein biosynthesis
bcl-2-Associated X Protein genetics
Apoptosis drug effects
Colonic Neoplasms drug therapy
Linolenic Acids pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 0250-7005
- Volume :
- 26
- Issue :
- 3A
- Database :
- MEDLINE
- Journal :
- Anticancer research
- Publication Type :
- Academic Journal
- Accession number :
- 16827117