p62/SQSTM1 is involved in caspase-8 associated cell death induced by proteasome inhibitor MG132 in U87MG cells.

Glioblastoma multiforme (GBM) is the most common and lethal type of brain cancer. Proteasome inhibitors are emerging as a new class of anti-glioma agents; however, the mechanisms of their killing malignant cells are still unclear. We treated U87MG cells with the proteasome inhibitor MG132 and found that cell death correlated with caspase-8 activation and autophagy protein p62/SQSTM1.

Autophagic degradation of caspase-8 protects U87MG cells against H2O2-induced oxidative stress.

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.

[Relationship between MC4R gene polymorphyism and body weight trait in beagle dogs].

The relationship between MC4R gene polymorphism and body weight in beagle dogs was analyzed. Using gene-specific primers based on canine MC4R exonic sequences a gene fragment was PCR amplified, cloned and sequenced to identify potential polymorphisms. The relationship between a MC4R gene polymorphism detected by PCR-RFLP and canine body weight was analyzed.