Nrf2 Deficiency Promotes Melanoma Growth and Lung Metastasis.

Reactive oxygen species (Apex, N.C.) Pub Date : 2016-01-01 Epub Date: 2016-05-30 DOI:10.20455/ros.2016.853
Hong Zhu, Zhenquan Jia, Michael A Trush, Y Robert Li
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Abstract

The role of Nrf2, a key regulator of antioxidant and cytoprotective genes, in tumorigenesis remains controversial. Here we showed that Nrf2 deficiency led to increased local tumor growth in mice following subcutaneous injection of B16-F10 melanoma cells, as indicated by increased proportion of animals with locally palpable tumor mass and time-dependent increases in tumor volume at the injection site. In vivo bioluminescence imaging also revealed increased growth of melanoma in Nrf2-null mice as compared with wild-type mice. By using a highly sensitive bioluminometric assay, we further found that Nrf2 deficiency resulted in a remarkable increase in lung metastasis of B16-F10 melanoma cells as compared with wild-type mice. Taken together, the results of this short communication for the first time demonstrated that Nrf2 deficiency promoted melanoma growth and lung metastasis following subcutaneous inoculation of B16-F10 cells in mice.

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Nrf2 缺陷促进黑色素瘤生长和肺转移
Nrf2是抗氧化和细胞保护基因的关键调节因子,它在肿瘤发生中的作用仍存在争议。在这里,我们发现,小鼠皮下注射 B16-F10 黑色素瘤细胞后,Nrf2 缺乏会导致局部肿瘤生长增加,表现为局部可触及肿瘤肿块的动物比例增加,以及注射部位肿瘤体积随时间增加。体内生物发光成像也显示,与野生型小鼠相比,Nrf2-null 小鼠体内黑色素瘤的生长速度加快。通过使用高灵敏度的生物发光测定法,我们进一步发现,与野生型小鼠相比,Nrf2 缺失导致 B16-F10 黑色素瘤细胞的肺转移显著增加。综上所述,这篇短文的研究结果首次证明了小鼠皮下接种B16-F10细胞后,Nrf2缺乏会促进黑色素瘤的生长和肺转移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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