Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 283, Issue 19, Pages 13174-13184Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M708008200
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- NCI NIH HHS [CA2 P30 CA076292-10, CA97950] Funding Source: Medline
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The human suppressor of morphogenesis in genitalia-1 (hSMG-1) protein kinase plays dual roles in mRNA surveillance and genotoxic stress response pathways in human cells. Here, we report that small interfering RNA-mediated depletion of hSMG-1, but not ATM, ATR, hUpf1, or hUpf2, in human U2OS osteosarcoma cells markedly increases the magnitude and accelerates the rate of apoptosis induced by tumor necrosis factor-alpha(TNF alpha) stimulation. The increase in TNF alpha-mediated cell killing observed in hSMG-1-depleted cells is not related to the suppression of nonsense-mediated mRNA decay or to the inhibition of TNF alpha-induced NF-kappa B activation. Rather, we observed that loss of hSMG-1 accelerates the degradation of the long form of the FLICE-inhibitory protein (FLIPL), an inhibitor of death-inducing signaling complex-mediated caspase-8 activation, in TNF alpha-treated cells. These results suggest that hSMG-1 plays an important role in cell survival during TNF alpha-induced stress.
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