High-Performance MoC Electrocatalyst for Hydrogen Evolution Reaction Enabled by Surface Sulfur Substitution.

Molybdenum carbides have been expected to be one of the promising catalysts for the hydrogen evolution reaction (HER) due to their similar d-band electronic structures to the Pt-group metals. However, the weaker hydrogen-adsorption ability of MoC severely hinders its applications. Guided by density functional theory calculations, we put forward a strategy to design the novel MoC-based electrocatalyst with surface reconstruction through sulfur doping. The incorporation of minor sulfur not only greatly increases the number of active sites and intrinsic activity but also optimizes the electronic structure to improve the electron transfer efficiency. As a result, the as-prepared sulfur-substituted MoC tackles the limitation of the Volmer step and exhibits superior HER performance with a small Tafel slope of 48 mV dec-1. Theoretical investigations demonstrate that the terminal sulfur plays a critical role in facilitating a close to zero hydrogen adsorption energy (ΔGH*) and a lower hydrogen release barrier.

MiR-1256 suppresses proliferation and migration of non-small cell lung cancer via regulating TCTN1.

Mounting evidence has shown that miRNA expression is abnormal in various human cancers. Here, we mainly explored the biological function and the potential mechanisms of miR-1256 in non-small cell lung cancer (NSCLC). The miR-1256 mRNA expression was detected by quantitative real-time PCR and tectonic family member 1 (TCTN1) mRNA expression was detected by immunoblotting. The TCTN1 was identified to be the direct and specific target gene of miR-1256 by luciferase reporter assay. Cell proliferation was examined by methyl thiazolyl tetrazolium assay and migration was detected by transwell assay. MiR-1256 expression was downregulated in NSCLC tissues, whereas the expression of TCTN1 was upregulated, compared with normal tissues. We also found that overexpression of miR-1256 in these NSCLC cell lines inhibited cell proliferation and migration. Furthermore, TCTN1 was identified as a direct target of miR-1256 by luciferase reporter assays. Collectively, these data stated that the inhibitory effect of miR-1256 in NSCLC was realized by upregulating TCTN1, suggesting that miR-1256/TCTN1 axis may play a critical role as NSCLC therapeutic target.