Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals

被引:33
|
作者
Tobe, Ryuta [1 ]
Carlson, Bradley A. [1 ]
Huh, Jang Hoe [2 ]
Castro, Nadia P. [3 ]
Xu, Xue-Ming [1 ,10 ]
Tsuji, Petra A. [4 ]
Lee, Sang-Goo [5 ]
Bang, Jeyoung [2 ]
Na, Ji-Woon [2 ]
Kong, Young-Yun [2 ]
Beaglehole, Daniel [1 ]
Southon, Eileen [6 ]
Seifried, Harold [7 ]
Tessarollo, Lino [8 ]
Salomon, David S. [3 ]
Schweizer, Ulrich [9 ]
Gladyshev, Vadim N. [5 ]
Hatfield, Dolph L. [1 ]
Lee, Byeong Jae [2 ]
机构
[1] NIH, Mol Biol Selenium, Mouse Canc Genet Program, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA
[2] Seoul Natl Univ, Sch Biol Sci, Seoul 151742, South Korea
[3] NIH, Tumor Growth Factor Sect, Mouse Canc Genet Program, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA
[4] Towson Univ, Dept Biol Sci, Towson, MD 21252 USA
[5] Harvard Med Sch, Brigham & Womens Hosp, Div Genet, Boston, MA 02115 USA
[6] NCI Frederick, Basic Sci Program, SAIC Frederick, Frederick, MD 21702 USA
[7] NCI, Nutr Sci Res Grp, Bethesda, MD 20892 USA
[8] NIH, Neural Dev Sect, Mouse Canc Genet Program, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA
[9] Rhein Friedrich Wilhelms Univ Bonn, Inst Biochem & Mol Biol, D-53115 Bonn, Germany
[10] Genecopoeia Inc, 9620 Med Ctr Dr 101, Rockville, MD 20850 USA
基金
美国国家卫生研究院; 新加坡国家研究基金会;
关键词
cancer; reactive oxygen species (ROS); redox regulation; selenium; selenocysteine; selenophosphate synthetase 1; SELENOPROTEIN BIOSYNTHESIS; GLUTATHIONE TRANSFERASE; THIOREDOXIN REDUCTASE; GENETIC-CODE; SELENOCYSTEINE; SELENIUM; METABOLISM; EXPRESSION; DROSOPHILA; CELLS;
D O I
10.1042/BCJ20160393
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Selenophosphate synthetase (SPS) was initially detected in bacteria and was shown to synthesize selenophosphate, the active selenium donor. However, mammals have two SPS paralogues, which are designated SPS1 and SPS2. Although it is known that SPS2 catalyses the synthesis of selenophosphate, the function of SPS1 remains largely unclear. To examine the role of SPS1 in mammals, we generated a Sps1-knockout mouse and found that systemic SPS1 deficiency led to embryos that were clearly underdeveloped by embryonic day (E)8.5 and virtually resorbed by E14.5. The knockout of Sps1 in the liver preserved viability, but significantly affected the expression of a large number of mRNAs involved in cancer, embryonic development and the glutathione system. Particularly notable was the extreme deficiency of glutaredoxin 1 (GLRX1) and glutathione transferase Omega 1 (GSTO1). To assess these phenotypes at the cellular level, we targeted the removal of SPS1 in F9 cells, a mouse embryonal carcinoma (EC) cell line, which affected the glutathione system proteins and accordingly led to the accumulation of hydrogen peroxide in the cell. Furthermore, we found that several malignant characteristics of SPS1-deficient F9 cells were reversed, suggesting that SPS1 played a role in supporting and/or sustaining cancer. In addition, the overexpression of mouse or human GLRX1 led to a reversal of observed increases in reactive oxygen species (ROS) in the F9 SPS1/GLRX1-deficient cells and resulted in levels that were similar to those in F9 SPS1-sufficient cells. The results suggested that SPS1 is an essential mammalian enzyme with roles in regulating redox homoeostasis and controlling cell growth.
引用
收藏
页码:2141 / 2154
页数:14
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