Large-area single-crystal TMD growth modulated by sapphire substrates.

Transition metal dichalcogenides (TMDs) have recently attracted extensive attention due to their unique physical and chemical properties; however, the preparation of large-area TMD single crystals is still a great challenge. Chemical vapor deposition (CVD) is an effective method to synthesize large-area and high-quality TMD films, in which sapphires as suitable substrates play a crucial role in anchoring the source material, promoting nucleation and modulating epitaxial growth. In this review, we provide an insightful overview of different epitaxial mechanisms and growth behaviors associated with the atomic structure of sapphire surfaces and the growth parameters. First, we summarize three epitaxial growth mechanisms of TMDs on sapphire substrates, namely, van der Waals epitaxy, step-guided epitaxy, and dual-coupling-guided epitaxy. Second, we introduce the effects of polishing, cutting, and annealing processing of the sapphire surface on the TMD growth. Finally, we discuss the influence of other growth parameters, such as temperature, pressure, carrier gas, and substrate position, on the growth kinetics of TMDs. This review might provide deep insights into the controllable growth of large-area single-crystal TMDs on sapphires, which will propel their practical applications in high-performance nanoelectronics and optoelectronics.

The antipsychotic drug penfluridol inhibits N-linked glycoprotein processing and enhances T-cell-mediated tumor immunity.

Aberrant N-linked glycosylation is a prominent feature of cancers. Perturbance of oligosaccharide structure on cell surfaces directly affects key processes in tumor development and progression. In spite of the critical role played by N-linked glycans in tumor biology, the discovery of small molecules that specifically disturbs the N-linked glycans is still under investigation. To identify more saccharide-structure-perturbing compounds, a repurposed drug screen by using a library consisting of 1530 FDA-approved drugs was performed. Interestingly, an antipsychotic drug, penfluridol, was identified as being able to decrease cell surface Wheat germ agglutinin (WGA) staining. In the presence of penfluridol, cell membrane glycoproteins PD-L1 shifted to a lower molecular weight. Further studies demonstrated that penfluridol treatment caused an accumulation of high-mannose oligosaccharides, especially Man5-7GlcNAc2 glycan structures. Mechanistically, this effect is due to direct targeting of MAN1A1 mannosidase, a Golgi enzyme involved in N-glycan maturation. Moreover, we found that altered glycosylation of PD-L1 caused by penfluridol disrupted interactions between PD-1 and PD-L1, resulting in activation of T-cell tumor immunity. In a mouse xenograft and glioma model, penfluridol enhanced the anti-tumor effect of the anti-PD-L1 antibody in vivo. Overall, these findings revealed an important biological activity of the antipsychotic drug penfluridol as an inhibitor of glycan processing and proposed a repurposed use of penfluridol in anti-tumor therapy through activation of T-cell immunity.

REC8 inhibits proliferation, migration and invasion of breast cancer cells by targeting CDC20.

Breast cancer is one of the most types of common malignant tumor in women. REC8 is a known tumor suppressor in several types of cancer; however, the role of REC8 in breast cancer remains unknown. The purpose of the present study was to investigate the effects and underlying mechanism of REC8 on the proliferation, migration and invasion of breast cancer cells. The expression of REC8 in normal and breast cancer cells was detected by reverse transcription­quantitative PCR and western blotting. Stable REC8­overexpressing breast cancer cells were constructed to modify the expression of REC8. The expression of cell division cycle 20 (CDC20) in breast cancer cells was altered using the CDC20 inhibitor apcin. Cell viability, proliferation, migration, invasion and apoptosis were determined by Cell Counting Kit­8, colony formation, wound healing, Transwell and TUNEL assays, respectively. Western blotting was performed to measure the expression of matrix metalloproteinase­2/9 and apoptosis­associated proteins [Bcl­2, caspase­3, cleaved caspase­3 and cleaved poly (ADP­ribose) polymerase]. Compared with normal breast cells, the expression of REC8 was lower in breast cancer cells. Search Tool for the Retrieval of Interacting Genes/Proteins online database was used to predict the interaction between REC8 and CDC20. Overexpression of REC8 significantly inhibited the proliferation, migration and invasion of breast cancer cells in vitro; these changes were reversed by CDC20 overexpression. In conclusion, the present study demonstrated that REC8 decreased proliferation, migration and invasion of breast cancer cells by inhibiting CDC20.