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방지영,허장호,나지운,Qiao Lu,Bradley A. Carlson,Ryuta Tobe,Petra A. Tsuji,Vadim N. Gladyshev,Dolph L. Hatfield,이병재 한국분자세포생물학회 2015 Molecules and cells Vol.38 No.5
The 15-kDa selenoprotein (Sep15) is a selenoprotein residing in the lumen of the endoplasmic reticulum (ER) and implicated in quality control of protein folding. Herein, we established an inducible RNAi cell line that targets Sep15 mRNA in Chang liver cells. RNAi-induced Sep15 deficiency led to inhibition of cell proliferation, whereas cell growth was resumed after removal of the knockdown inducer. Sep15-deficient cells were arrested at the G1 phase by upregulating p21 and p27, and these cells were also characterized by ER stress. In addition, Sep15 deficiency led to the relocation of focal adhesions to the periphery of the cell basement and to the decrease of the migratory and invasive ability. All these changes were reversible depending on Sep15 status. Rescuing the knockdown state by expressing a silent mutant Sep15 mRNA that is resistant to siRNA also reversed the phenotypic changes. Our results suggest that SEP15 plays important roles in the regulation of the G1 phase during the cell cycle as well as in cell motility in Chang liver cells, and that this selenoprotein offers a novel functional link between the cell cycle and cell motility.
Salvador Naranjo-Suarez,Dolph L. Hatfield,Bradley A. Carlson,Ryuta Tobe,유민혁,Petra A. Tsuji,Vadim N. Gladyshev 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.2
Under hypoxic conditions, cells activate a transcriptional response mainly driven by hypoxia-inducible factors (HIFs). HIF-1 stabilization and activity are known to be regulated by thioredoxin 1 (Txn1), but how the thioredoxin system regulates the hypoxic response is unknown. By examining the effects of Txn1 overexpression on HIF-1 function in HeLa, HT-29, MCF-7 and EMT6 cell lines, we found that this oxidoreductase did not stabilize HIF-1, yet could increase its activity. These effects were dependent on the redox function of Txn1. However, Txn1 deficiency did not affect HIF-1 hypoxic-stabilization and activity, and overexpression of thioredoxin reductase 1 (TR1), the natural Txn1 reductase, had no influence on HIF-1 activity. Moreover, overexpression of Txn1 in TR1 deficient HeLa and EMT6 cells was still able to increase HIF-1 hypoxic activity. These results indicate that Txn1 is not essential for HIF-1 hypoxic stabilization or activity, that its overex-pression can increase HIF-1 hypoxic activity, and that this effect is observed regardless of TR1 status. Thus, regulation of HIF-1 by the thioredoxin system depends on the specific levels of this system’s major components.
Bang, Jeyoung,Huh, Jang Hoe,Na, Ji-Woon,Lu, Qiao,Carlson, Bradley A.,Tobe, Ryuta,Tsuji, Petra A.,Gladyshev, Vadim N.,Hatfield, Dolph L.,Lee, Byeong Jae Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.5
The 15-kDa selenoprotein (Sep15) is a selenoprotein residing in the lumen of the endoplasmic reticulum (ER) and implicated in quality control of protein folding. Herein, we established an inducible RNAi cell line that targets Sep15 mRNA in Chang liver cells. RNAi-induced Sep15 deficiency led to inhibition of cell proliferation, whereas cell growth was resumed after removal of the knockdown inducer. Sep15-deficient cells were arrested at the G1 phase by upregulating p21 and p27, and these cells were also characterized by ER stress. In addition, Sep15 deficiency led to the relocation of focal adhesions to the periphery of the cell basement and to the decrease of the migratory and invasive ability. All these changes were reversible depending on Sep15 status. Rescuing the knockdown state by expressing a silent mutant Sep15 mRNA that is resistant to siRNA also reversed the phenotypic changes. Our results suggest that SEP15 plays important roles in the regulation of the G1 phase during the cell cycle as well as in cell motility in Chang liver cells, and that this selenoprotein offers a novel functional link between the cell cycle and cell motility.