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

作者:Yang, Lijun; Yuan, Jianlin; Liu, Liwen; Shi, Changhong; Wang, Longxin; Tian, Feng; Liu, Fei; Wang, He; Shao, Chen; Zhang, Qiang; Chen, Zhinan; Qin, Weijun*; Wen, Weihong
来源:Oncology Letters, 2013, 6(1): 197-202.
DOI:10.3892/ol.2013.1336

摘要

omega-3 fatty acids have potential anticancer effects, and consuming food rich in omega-3 fatty acids reduces the human renal cell carcinoma (RCC) risk. However, the direct effect of omega-3 fatty acids on RCC in vitro is unknown. In the present study, the effects of alpha-linolenic acid (ALA), an omega-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-gamma (receptor-gamma) 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 mu M) dose-dependently suppressed the proliferation of the OS-RC-2 cells. PPAR-gamma activity and gene expression were significantly increased by ALA at 20 and 40 mu M. COX-2 activity and gene expression levels were significantly decreased by ALA from 20 mu M. Use of purely the PPAR-gamma 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-gamma activation and COX-2 inhibition serve as two signaling pathways for the inhibitory effects of ALA on RCC cell proliferation.