Anti-SIRT5 (aa 9-286) polyclonal antibody

SUN2, a key component of LINC (linker of nucleoskeleton and cytoskeleton) complex located at the inner nuclear membrane, plays unknown role in lung cancer. We found that SUN2 expression was decreased in lung cancer tissue compared with paired normal tissues and that higher SUN2 levels predicted better overall survival and first progression survival. Overexpression of SUN2 inhibits cell proliferation, colony formation and migration in lung cancer, whereas knockdown of SUN2 promotes cell proliferation and migration. Additionally, SUN2 increases the sensitivity of lung cancer to cisplatin by inducing cell apoptosis. Mechanistically, we showed that SUN2 exerts its tumor suppressor functions by decreasing the expression of GLUT1 and LDHA to inhibit the Warburg effect. Finally, our results provided evidence that SIRT5 acts, at least partly, as a negative regulator of SUN2. Taken together, our findings indicate that SUN2 is a key component in lung cancer progression by inhibiting the Warburg effect and that the novel SIRT5/SUN2 axis may prove to be useful for the development of new strategies for treating the patients with lung cancer.

Human exposure to phthalates has received special attention due to their possible adverse human health effects. Diisononyl phthalate (DINP) is a plasticizer still widely used in many products, despite being considered an endocrine disruptor. In this study, we evaluated DINP's cytotoxicity, its effect on the levels of reactive oxygen species (ROS), and its effect on sirtuin expression in HepG2 cells. Results showed that 1 mu g/mL DINP significantly downregulated Sirt1, Sirt2, Sirt3, and Sirt5 gene expression (p < 0.05), while other sirtuins remained unaffected. Furthermore, protein levels of Sirt1 and Sirt3 were significantly downregulated by 1 mu g/mL DINP. On the other hand, 100 mu g/mL DINP doubled the levels of lysine acetylation proteins (increased 2-fold) as well as reactive oxygen species (ROS) compared with the controls. In conclusion, our study suggests, for the first time, that DINP regulates the potential epigenetic disruptor sirtuin family and leads to induction of ROS via sirtuins.