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Oxidative stress induces apoptosis in many cellular systems including glioblastoma cells, with caspase-8 activation was regarded as a major contribution to H2O2-induced cell death. This study focused on the role of the autophagic protein p62 in H2O2-induced apoptosis in U87MG cells. Oxidative stress was applied with H2O2, and cell apoptosis and viability were measured with use of caspase inhibitors or autophagic mediators or siRNA p62, GFP-p62 and GFP-p62-UBA (del) transfection. We found that H2O2 -induced U87MG cell death was correlated with caspase-8. To understand the role of p62 in MG132-induced cell death, the levels of p62/SQSTM1 or autophagy in U87MG cells were modulated with biochemical or genetic methods. The results showed that the over-expression of wild type p62/SQSTM1 significantly reduced H2O2 induced cell death, but knockdown of p62 aggravated the process. In addition, inhibition of autophagy promoted p62 and active caspase-8 increasing H2O2 -induced apoptosis while induction of autophagy manifested the opposite effect. We further demonstrated that the function of p62/SQSTM1 required its C-terminus UBA domain to attenuate H2O2 cytotoxity by inhibition of caspase-8 activity. Our results indicated that p62/SQSTM1 was a potential contributor to mediate caspase-8 activation by autophagy in oxidative stress process.

Autophagic Degradation of Caspase-8 Protects U87MG Cells Against H2O2-induced Oxidative Stress

Autophagic Degradation of Caspase-8 Protects U87MG Cells Against H₂O₂-induced Oxidative Stress