High-Efficiency Capture of Cells by Softening Cell Membrane.

The capture of circulating tumor cells (CTCs) by nanostructured substrate surface is a useful method for early diagnosis of cancer. At present, most methods used to improve the cell capture efficiency are based on changing substrate surface properties. However, there are still some gaps between these methods and practical applications. Here, a method is presented for improving cell capture efficiency from a different perspective, that is, changing the properties of the cells. Concretely, the mechanical properties of the cell membrane are changed by adding Cytochalasin D to soften the cell membrane. Furthermore, a corresponding theoretical model is proposed to explain the experimental results. It is found that cell softening can reduce the resistance of cell adhesion, which makes the adhesion ability stronger. The high-efficiency capture of cells by softening the cell membrane provides a potential method to improve the detection performance of CTCs.

Sirt3 activates autophagy to prevent DOX-induced senescence by inactivating PI3K/AKT/mTOR pathway in A549 cells.

Sirtuin 3 (Sirt3), a mitochondrial deacetylase, regulates mitochondrial redox homeostasis and autophagy and is involved in physiological and pathological processes such as aging, cellular metabolism, and tumorigenesis. We here investigate how Sirt3 regulates doxorubicin (DOX)-induced senescence in lung cancer A549 cells. Sirt3 greatly reduced DOX-induced upregulation of senescence marker proteins p53, p16, p21 and SA-ß-Gal activity as well as ROS levels. Notably, Sirt3 reversed DOX-induced autophagic flux blockage, as shown by increased p62 degradation and LC3II/LC3I ratio. Importantly, the autophagy inhibitors 3-methyladenine (3-MA) and chloroquine (CQ) partially abolished the antioxidant stress and antiaging effects of Sirt3, while the autophagy activator rapamycin (Rap) potentiated these effects of Sirt3, demonstrating that autophagy mediates the anti-aging effects of Sirt3. Additionally, Sirt3 inhibited the DOX-induced activation of the phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway, which in turn activated autophagy. The PI3K inhibitor LY294002 promoted the antioxidant stress and antiaging effects of Sirt3, while the AKT activator SC-79 reversed these effects of Sirt3. Taken together, Sirt3 counteracts DOX-induced senescence by improving autophagic flux.