Endogenously synthesized n-3 polyunsaturated fatty acids in fat-1 transgenic mice suppress B16F10 melanoma lung metastasis by impairing mesenchymal to epithelial transition

Endogenously synthesized n-3 polyunsaturated fatty acids in fat-1 transgenic mice suppress B16F10 melanoma lung metastasis by impairing mesenchymal to epithelial transition
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fat-1转基因小鼠内源合成的n-3多不饱和脂肪酸通过损害间充质到上皮的转化来抑制B16F10黑色素瘤肺转移

DOI:
10.1016/j.jff.2016.10.006
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发表时间:
2016-12
影响因子:
5.6
通讯作者:
Bu Shi-Zhong
Bu Shi-Zhong
中科院分区:
农林科学2区
文献类型:
--
作者:
Zhu Pan;Zhang Yuan-Ming;Yin Xuan;Zhang Xiao-Hong;Wang Feng;Zhang Jin-Jie;Yan Wang;Xi Yang;Wan Jian-Bo;Kang Jing-Xuan;Zou Zu-Quan;Bu Shi-Zhong

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Malignant melanoma is an aggressive cancer of neuroectodermal origin. The mechanisms of n-3 polyunsaturated fatty acids (PUFAs) against melanoma metastasis are not clear. Here fat-1 and wild type (WT) mice were injected with B16F10 melanoma cells via the tail vein to establish lung metastasis model. Endogenous n-3 PUFAs were associated with a reduction in grossly visible pulmonary metastases and outgrowth through inhibition of mesenchymal to epithelial transition (MET), which was characterized by decreased expression of epithelial markers E-cadherin and ZO-1, and increased expression of mesenchymal marker vimentin in tumour tissues from fat-1 mice compared with WT controls. In addition, n-3 PUFA-mediated inhibition of MET may have been associated, in part, with the: (i) formation of n-3 PUFA-derived lipid mediators and (ii) decreased expression of mature IL-1β and p-NF-κB, and enhanced expression of superoxide dismutase-1. These results suggest that n-3 PUFAs exert their antitumourigenic activities, in part, via their anti-inflammatory properties.
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