Oncol Lett, 2013, Volume 6; Issue 1:Pages 197 - 202

Alpha linolenic acid inhibits human renal cell carcinoma cell proliferation through PPARy activation and COX2 inhibition

Yang, L. Yuan, J. Liu, L. Shi, C. Wang, L. Tian, F. Liu, F. Wang, H. et al

Key Findings

ALA inhibited the proliferation of OS RC 2 cells, a human renal cancer cell line.  The mechanism may be through an increase PPARg activity and gene expression. Together with the PPARg agonist, ALA decreased cell proliferation. In addition, ALA inhibited COX 2 which is a carcinogenesis and a pro- inflammatory compound.  ALA which regulates the activities of PPARg and COX 2 may be relevant for RCC therapy.

ABSTRACT

: n3 fatty acids have potential anticancer effects, and consuming food rich in n3 fatty acids reduces the human renal cell carcinoma (RCC) risk. However, the direct effect of n3 fatty acids on RCC in vitro is unknown. In the present study, the effects of alpha linolenic acid (ALA), an n3 fatty acid, were observed on cell proliferation in the RCC cell line OS  RC  2. The activity and gene expression levels of peroxisome proliferators activated receptor gamma  (PPARg) and cyclooxygenase 2 (COX 2) in the OS RC 2 cells were measured by ELISA and real time R PCR, respectively, following ALA treatment. ALA (20 to 80 microM) dose dependently suppressed the proliferation of the OS RC 2 cells. PPARg activity and gene expression were significantly increased by ALA at 20 and 40 microM. COX  2 activity and gene expression levels were significantly decreased by ALA from 20 microM. Use of purely the PPARg agonist, rosiglitazone, decreased the proliferation of the OS RC 2 cells, while ALA induced further suppression of cell proliferation in the presence of rosiglitazone. The COX 2 inhibitor N (3 Pyridyl)indomethacinamide induced further suppression of cell proliferation in the presence of rosiglitazone. N (3 Pyridyl) indomethacinamide also suppressed the proliferation of the OS RC2 cells. In the presence of N (3 Pyridyl) indomethacinamide, ALA and rosiglitazone further inhibited OS RC 2 cell proliferation. In conclusion, ALA inhibits the cell proliferation of the OS RC 2 human RCC cell line. PPARg activation and COX 2 inhibition serve as two signaling pathways for the inhibitory effects of ALA on RCC cell proliferation. (Authors abstract)

 

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