Cell Proliferation and Motility Are Inhibited by G1 Phase Arrest in 15-kDa Selenoprotein-Deficient Chang Liver Cellsстатья
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Дата последнего поиска статьи во внешних источниках: 10 декабря 2018 г.
Аннотация: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.