| First Author | Yin X | Year | 2016 |
| Journal | Mol Med Rep | Volume | 14 |
| Issue | 4 | Pages | 3476-84 |
| PubMed ID | 27573698 | Mgi Jnum | J:290201 |
| Mgi Id | MGI:6433019 | Doi | 10.3892/mmr.2016.5639 |
| Citation | Yin X, et al. (2016) Endogenously synthesized n-3 fatty acids in fat-1 transgenic mice prevent melanoma progression by increasing E-cadherin expression and inhibiting beta-catenin signaling. Mol Med Rep 14(4):3476-84 |
| abstractText | Malignant melanoma is the most lethal form of skin cancer. Although preclinical studies have shown that n-3 polyunsaturated fatty acids (PUFAs) are beneficial for prevention of melanoma, the molecular mechanisms underlying the protective effects of n3 PUFAs on melanoma remain largely unknown. In the present study, endogenously increased levels of n-3 PUFAs in the tumor tissues of omega3 fatty acid desaturase (fat1) transgenic mice was associated with a reduction in the growth rate of melanoma xenografts. This reduction in tumor growth in fat1 mice compared with wildtype controls may have been associated, in part, to the: i) Increased expression of Ecadherin and the reduced expression of its transcriptional repressors, the zinc finger Ebox binding homeobox 1 and snail family transcriptional repressor 1; ii) significant repression of the epidermal growth factor receptor/Akt/betacatenin signaling pathway; and iii) formation of significant levels of n3 PUFAderived lipid mediators, particularly resolvin D2 and E1, maresin 1 and 15hydroxyeicosapentaenoic acid. In addition, vitamin E administration counteracted n3 PUFAinduced lipid peroxidation and enhanced the antitumor effect of n3 PUFAs, which suggests that the protective role of n3 PUFAs against melanoma is not mediated by n3 PUFAsinduced lipid peroxidation. These results highlight a potential role of n3 PUFAs supplementation for the chemoprevention of melanoma in highrisk individuals, and as a putative adjuvant agent in the treatment of malignant melanoma. |
