Cell Proliferation and Motility Are Inhibited by G1 Phase Arrest in 15-kDa Selenoprotein-Deficient Chang Liver Cells

DSpace/Manakin Repository

Cell Proliferation and Motility Are Inhibited by G1 Phase Arrest in 15-kDa Selenoprotein-Deficient Chang Liver Cells

Citable link to this page

 

 
Title: Cell Proliferation and Motility Are Inhibited by G1 Phase Arrest in 15-kDa Selenoprotein-Deficient Chang Liver Cells
Author: 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

Note: Order does not necessarily reflect citation order of authors.

Citation: Bang, Jeyoung, Jang Hoe Huh, Ji-Woon Na, Qiao Lu, Bradley A. Carlson, Ryuta Tobe, Petra A. Tsuji, Vadim N. Gladyshev, Dolph L. Hatfield, and Byeong Jae Lee. 2015. “Cell Proliferation and Motility Are Inhibited by G1 Phase Arrest in 15-kDa Selenoprotein-Deficient Chang Liver Cells.” Molecules and Cells 38 (5): 457-465. doi:10.14348/molcells.2015.0007. http://dx.doi.org/10.14348/molcells.2015.0007.
Full Text & Related Files:
Abstract: 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.
Published Version: doi:10.14348/molcells.2015.0007
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4443288/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:17295737
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters