High-Performance Two-Dimensional Electronics with a Noncontact Remote Doping Method.

Because of the intrinsic low carrier density of monolayer two-dimensional (2D) materials, doping is crucial for the performance of underlap top-gated 2D devices. However, wet etching of a high-k (dielectric constant) dielectric layer is difficult to implement without causing performance deterioration on the devices; therefore, finding a suitable spacer doping technique for 2D devices is indispensable. In this study, we developed a remote doping (RD) method in which defective SiOx can remotely dope the underlying high-k capped 2D regions without directly contacting these materials. This method achieved a doping density as high as 1.4 × 1013 cm-2 without reducing the mobility of the doped materials; after 1 month, the doping concentration remained as high as 1.2 × 1013 cm-2. Defective SiOx can be used to dope most popular 2D transition-metal dichalcogenides. The low-k properties of SiOx render it ideal for spacer doping, which is very attractive from the perspective of circuit operation. In our experiments, MoS2 and WS2 underlap top-gate devices exhibited 10× and 200× increases in their on-currents, respectively, after being doped with SiOx. These results indicate that SiOx doping can be conducted to manufacture high-performance 2D devices.

USP24 induces IL-6 in tumor-associated microenvironment by stabilizing p300 and ß-TrCP and promotes cancer malignancy.

We have previously demonstrated that USP24 is involved in cancer progression. Here, we found that USP24 expression is upregulated in M2 macrophages and lung cancer cells. Conditioned medium from USP24-knockdown M2 macrophages decreases the migratory and chemotactic activity of lung cancer cells and the angiogenic properties of human microvascular endothelial cell 1 (HMEC-1). IL-6 expression is significantly decreased in USP24-knockdown M2 macrophages and lung cancer cells, and IL-6-replenished conditioned medium restores the migratory, chemotactic and angiogenetic properties of the cells. USP24 stabilizes p300 and ß-TrCP to increase the levels of histone-3 acetylation and NF-κB, and decreases the levels of DNMT1 and IκB, thereby increasing IL-6 transcription in M2 macrophages and lung cancer cells, results in cancer malignancy finally. IL-6 has previously been a target for cancer drug development. Here, we provide direct evidence to support that USP24 promotes IL-6 expression, which might be beneficial for cancer therapy.