Work

α-linolenic acid inhibits human renal cell carcinoma cell proliferation through PPAR-γ activation and COX-2 inhibition

Year: 2013

Type: article

Abstract: ω‑3 fatty acids have potential anticancer effects, and consuming food rich in ω‑3 fatty acids reduces the human renal cell carcinoma (RCC) risk. However, the direct effect of ω‑3 fatty acids on RCC in vitro is unknown. In the present study, the effects of α‑linolenic acid (ALA), an ω‑3 fatty acid, were observed on cell proliferation in the RCC cell line OS‑RC‑2. The activity and gene expression levels of peroxisome proliferator‑activated receptor‑γ (PPAR‑γ) and cyclooxygenase‑2 (COX‑2) in the OS‑RC‑2 cells were measured by ELISA and real‑time RT‑PCR, respectively, following ALA treatment. ALA (20‑80 µM) dose‑dependently suppressed the proliferation of the OS‑RC‑2 cells. PPAR‑γ activity and gene expression were significantly increased by ALA at 20 and 40 µM. COX‑2 activity and gene expression levels were significantly decreased by ALA from 20 µM. Use of purely the PPAR‑γ 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‑RC‑2 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. PPAR‑γ activation and COX‑2 inhibition serve as two signaling pathways for the inhibitory effects of ALA on RCC cell proliferation.

Source: Oncology Letters

DOI: 10.3892/ol.2013.1336