Surface dynamics at photoactive liquid crystal polymer networks

\u3cp\u3eThe field of advanced and responsive soft materials is at the edge of a new era. After several decades during which liquid crystals generated new functions for information displays and could solve many problems in emerging fields such as (tele)communications, this material system is being utilized to reach out to completely new application fields with functions that can take over biological actions (cell growth and manipulation), change the way materials, machines, or robots interact with humans (haptics), and modulate surface properties, e.g., tribology and wettability. This Progress Report concentrates on creating surface movement in liquid crystal networks with an emphasis on the light-responsive dynamic surface topographies that transfer from a flat to a predesigned corrugated state via light illumination, e.g., UV and visible light. Within this framework, the interaction between dynamic surfaces and the environment, such as controlled friction, wettability, and material transport, are illustrated. In addition, the light-induced thermal effect is discussed. The article concludes with the existing challenges and an outlook on the opportunities.\u3c/p\u3

Genomic and Functional Analysis of the E3 Ligase PARK2 in Glioma

PARK2 (PARKIN) is an E3 ubiquitin ligase whose dysfunction has been associated with the progression of Parkinsonism and human malignancies, and its role in cancer remains to be explored. In this study, we report that PARK2 is frequently deleted and underexpressed in human glioma, and low PARK2 expression is associated with poor survival. Restoration of PARK2 significantly inhibited glioma cell growth both in vitro and in vivo, whereas depletion of PARK2 promoted cell proliferation. PARK2 attenuated both Wnt- and EGF-stimulated pathways through downregulating the intracellular level of β-catenin and EGFR. Notably, PARK2 physically interacted with both β-catenin and EGFR. We further found that PARK2 promoted the ubiquitination of these two proteins in an E3 ligase activity-dependent manner. Finally, inspired by these newly identified tumor-suppressive functions of PARK2, we tested and proved that combination of small-molecule inhibitors targeting both Wnt-β-catenin and EGFR-AKT pathways synergistically impaired glioma cell viability. Together, our findings uncover novel cancer-associated functions of PARK2 and provide a potential therapeutic approach to treat glioma