Eicosapentaenoic acid induced SKOV-3 cell apoptosis through ERK1/2–mTOR–NF-κB pathways. Issue 7 (August 2016)

• Record Type: Journal Article
• Authors: Han, Lirong; Zhang, Yuanyuan; Meng, Meng; Cheng, Dai; Wang, Chunling
• Is Part Of: Anti-cancer drugs. Volume 27:Issue 7(2016)
• Publication Date: 2016-08
• Subjects: apoptosis -- eicosapentaenoic acid -- ERK1/2 -- mTOR -- SKOV-3 cells; Antineoplastic agents -- Periodicals; Cancer -- Chemotherapy -- Periodicals; Antineoplastic Agents -- therapeutic use -- Periodicals; Drug Therapy -- Periodicals; 616.994061
• DOI: 10.1097/CAD.0000000000000373
• Languages: English
• ISSNs: 0959-4973

Abstract

Abstract : Eicosapentaenoic acid (EPA), a typical kind of n -3 polyunsaturated fatty acids, has been considered to be a potent antitumor adjuvant. However, the mechanism related to EPA-induced SKOV-3 cell apoptosis has not been investigated. In this study, we elucidated the anticancer effect of EPA on SKOV-3 cells and its molecular mechanisms. The results of fluorescence microscopy showed that EPA induced typical apoptotic morphological features in SKOV-3 cells. Flow cytometric analysis indicated that EPA induced apoptosis of SKOV-3 cells through cells arrested at the S phase. Western blotting results showed that EPA could inhibit the phosphorylation of ERK1/2 and Akt, which restrained mammalian target of rapamycin (mTOR) phosphorylated. Simultaneously, EPA downregulated the phosphorylation status of mTOR, which may act as an upstream regulator of EPA-blocked nuclear factor κB (NF-κB) p65 translocation from the cytoplasm into the nucleus; the apoptotic mechanism of SKOV-3 cells induced by EPA was associated with the release of cytochrome c, Bax-to-Bcl-2 expression ratio, and activation of caspase-3 and caspase-9. The results suggested that EPA induced SKOV-3 cell apoptosis through ERK1/2, Akt–mTOR–NF-κB pathways. Abstract : Supplemental Digital Content is available in the text.