Tungsten oxide (WO3) is a wide band gap semiconductor with unintentionally n−doping performance, excellent conductivity, and high electron hall mobility, which is considered as a candidate material for application in optoelectronics. Several reviews on WO3 and its derivatives for various applications dealing with electrochemical, photoelectrochemical, hybrid photocatalysts, electrochemical energy storage, and gas sensors have appeared recently. Moreover, the nanostructured transition metal oxides have attracted considerable attention in the past decade because of their unique chemical, photochromic, and physical properties leading to numerous other potential applications. Owing to their distinctive photoluminescence (PL), electrochromic and electrical properties, WO3 nanostructure−based optical and electronic devices application have attracted a wide range of research interests. This review mainly focuses on the up−to−date progress in different advanced strategies from fundamental analysis to improve WO3 optoelectric, electrochromic, and photochromic properties in the development of tungsten oxide−based advanced devices for optical and electronic applications including photodetectors, light−emitting diodes (LED), PL properties, electrical properties, and optical information storage. This review on the prior findings of WO3−related optical and electrical devices, as well as concluding remarks and forecasts will help researchers to advance the field of optoelectric applications of nanostructured transition metal oxides.
Ribosomal protein s15a (RPS15A), a highly conserved cytoplasmic protein, promotes mRNA/ribosome interaction in translation. Recent evidence showed that RPS15A is essential for tumor growth. RPS15A expression level was measured in glioblastoma tissue samples and normal brain (NB) tissue samples. RPS15A RNAi stable cell line U87 and U251 was generated by the pLVTHM-GFP lentiviral RNAi expression system. The knockdown efficiency was confirmed by quantitative real-time PCR and western blot. Molecular mechanisms and the effect of RPS15A on cell growth and migration were investigated by using western blot, MTT assay, wound healing assay, transwell migration assay, and tumorigenesis in nude mice. Here, we report that RPS15A is overexpressed in human glioblastoma tumor tissues. RPS15A knockdown inhibits proliferation and migration of glioblastoma cells in vitro. Knocking down RPS15A leads to the level of p-Akt decrease and cell cycle arrested in G0/G1 phase in U87 and U251 cells. Furthermore, the growth of glioblastoma cell-transplanted tumors in nude mice is inhibited by transduction with Lv-shRPS15A. Our findings indicate that RPS15A promotes cell proliferation and migration in glioblastoma for the first time. RPS15A might play a distinct role in glioblastoma and serve as a potential target for therapy.
Background: Glioblastoma (GBM) is the most common and most aggressive form of brain cancer. After surgery, radiotherapy is the mainstay of treatment for GBM patients. Unfortunately, the vast majority of GBM patients fail responding to radiotherapy because GBM cells remain highly resistant to radiation. Radiotherapy-induced DNA damage response may correlate with therapeutic resistance. Methods: Ionizing radiation (IR) was used to induce DNA damage. Cell proliferation and migration were detected by wound-healing, MTT and apoptosis assays. Dual-luciferase assays and Western blot analysis were performed to evaluate NF-κB activation and validate microRNA targets. Real-time PCR was used to study mRNA and microRNA levels. Results: IR-induced DNA damage activated NF-κB in GBM cells which promoted expression of IL-6, IL-8 and Bcl-xL, thereby contributing to cell survival and invasion. Knockdown SENP2 expression enhanced NF-κB essential modulator (NEMO) SUMOylation and NF-κB activity following IR exposure. miR-181b targets SENP2 and positively regulated NF-κB activity. Conclusion: NF-κB activation by DNA damage in GBM cells confers resistance to radiation-induced death.
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