Tunable Schottky barrier in InTe/graphene van der Waals heterostructure.

The structures and electronic properties of InTe/graphene van der Waals heterostructures are systematically investigated using the first-principles calculations. The electronic properties of InTe monolayer and graphene are well preserved respectively and the bandgap energy of graphene is opened to 36.5 meV in the InTe/graphene heterostructure. An n-type Schottky contact is formed in InTe/graphene heterostructure at the equilibrium state. There is a transformation between n-type and p-type Schottky contact when the interlayer distance is smaller than 3.56 Å or the applied electric field is larger than -0.06 V Å-1. In addition, the Schottky contact converts to Ohmic contact when the applied vertical electric field is larger than 0.11 V Å-1 or smaller than -0.13 V Å-1.

Schottky barrier modulation of a GaTe/graphene heterostructure by interlayer distance and perpendicular electric field.

Two-dimensional materials have recently been the focus of extensive research. Graphene-based vertical van der Waals heterostructures are expected to design and fabricate novel electronic and optoelectronic devices. Monolayer gallium telluride is a graphene-like nanosheet synthesized in experiment. Here, the electronic properties of GaTe/graphene heterostructures are investigated under the interlayer coupling and the applied perpendicular electric field. The results show that the electronic properties of GaTe and graphene are preserved, and the energy bandgap of graphene is opened to 13.5 meV in the GaTe/graphene heterostructure. It is found that the n-type Schottky contact is formed in the GaTe/graphene heterostructure, which can be tuned by the interlayer coupling, and the applied electric field. Moreover, a transformation from n-type to p-type Schottky contact is observed when the interlayer distance is smaller than 3.15 Å or the applied electric field is larger than 0.05 V Å-1. These properties are fundamental to the design of new Schottky nanodevices based on the GaTe/graphene heterostructure.

Tuning Electronic Properties of Blue Phosphorene/Graphene-Like GaN van der Waals Heterostructures by Vertical External Electric Field.

The structural and electronic properties of a monolayer and bilayer blue phosphorene/graphene-like GaN van der Waals heterostructures are studied using first-principle calculations. The results show that the monolayer-blue phosphorene/graphene-like GaN heterostructure is an indirect bandgap semiconductor with intrinsic type II band alignment. More importantly, the external electric field tunes the bandgap of monolayer-blue phosphorene/graphene-like GaN and bilayer-blue phosphorene/graphene-like GaN, and the relationship between bandgap and external electric field indicates a Stark effect. The semiconductor-to-metal transition is observed in the presence of a strong electric field.

MicroRNA­1915­3p prevents the apoptosis of lung cancer cells by downregulating DRG2 and PBX2.

Micro (mi)RNAs are short non­coding RNA molecules, which post­transcriptionally regulate gene expression and exert key roles in cell growth, differentiation and apoptosis. In the present study, the mechanism and the function of miR­1915­3p in the apoptotic regulation of lung cancer cell lines (NCI­H441 and NCI­H1650) were investigated. The expression analysis confirmed that the expression of miR­1915­3p was markedly decreased in the apoptotic cells. The overexpression of miR­1915­3p in the lung cancer cells prevented apoptosis induced by etoposide. Developmentally regulated GTP­binding protein 2 (DRG2) and pre­B cell leukemia homeobox 2 (PBX2) were identified as downstream targets of miR­1915­3p, which was shown to bind directly to the 3'­untranslated region of DRG2 and PBX2, subsequently lowering their mRNA and protein expression levels. Co­expression of miR­1915­3p and DRG2/PBX2 in the NCI­H441 and NCI­H1650 cells partly circumvented the effect of miR­1915­3p on apoptosis. The results in the present study revealed that miR­1915­3p functions as a silencer of apoptosis, which regulates lung cancer apoptosis via targeting DRG2/PBX2, and consequently this miRNA may be a putative therapeutic target in lung cancer.

MiRNA-1469 promotes lung cancer cells apoptosis through targeting STAT5a.

MicroRNAs play key roles in cell growth, differentiation, and apoptosis. In this study, we described the regulation and function of miR-1469 in apoptosis of lung cancer cells (A549 and NCI-H1650). Expression analysis verified that miR-1469 expression significantly increased in apoptotic cells. Overexpression of miR-1469 in lung cancer cells increased cell apoptosis induced by etoposide. Additionally, we identified that Stat5a is a downstream target of miR-1469, which can bind directly to the 3'-untranslated region of the Stat5a, subsequently reducing both the mRNA and protein levels of Stat5a. Finally, co-expression of miR-1469 and Stat5a in A549 and NCI-H1650 cells partially abrogated the effect of miR-1469 on cell apoptosis. Our results show that miR-1469 functions as an apoptosis enhancer to regulate lung cancer apoptosis through targeting Stat5a and may become a critical therapeutic target in lung cancer.