Hsa_circ_0005050 regulated the progression of oral squamous cell carcinoma via miR-487a-3p/CHSY1 axis.

Background/purpose: Circular RNAs (circRNAs) have been identified as potential functional modulators of the cellular physiology processes. This study aims to learn the potential molecular mechanisms of hsa_circ_0005050 (circ_0005050) in oral squamous cell carcinoma (OSCC). Materials and methods: Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was used to examine the expression of circ_0005050, miR-487a-3p, and chondroitin sulfate synthase 1 (CHSY1). Dual-luciferase reporter system, RNA pull-down, and RNA Immunoprecipitation (RIP) assays were used to determine the binding between miR-487a-3p and circ_0005050 or CHSY1. Colony formation experiment and EdU assay were used to investigate proliferation. Wound-healing and transwell assays were used to detect the migration of cells. The apoptosis rate of OSCC cells was tested by flow cytometry. Protein levels of related factors were determined by Western blot. Tumor xenograft was established to determine the regulatory role of circ_0005050 on tumor growth in vivo, and Ki-67 expression was detected in this xenograft using Immunohistochemical (IHC). Results: We implicated that circ_0005050 was apparently upregulated in OSCC tissues cells. In function experiments, repressing of circ_0005050 remarkably retarded OSCC growth in vitro. Furthermore, we conducted dual-luciferase reporter assays and RNA pull-down assays to verify that circ_0005050 sponged miR-487a-3p. Suppression of miR-487a-3p rescued the inhibition of proliferation in SCC15 and SCC25 cells induced by circ_0005050 knockdown. In addition, we found that overexpression of CHSY1 also reversed the inhibitory effect of circ_0005050 silencing on cell proliferation. Moreover, circ_0005050 knockdown inhibited tumor growth in vivo. Conclusion: Circ_0005050 acted as an oncogenic factor in OSCC progression through miR-487a-3p/CHSY1 axis.

Circ_0014359 promotes oral squamous cell carcinoma progression by sponging miR-149.

This study aimed to explore the role and mechanism of circ_0014359 in the OSCC. We firstly investigated the expression levels of circ_0014359 in OSCC tissues and cell lines. Then, the effects of knocking down circ_0014359 on cellular viability, apoptosis, migration, and invasion of OSCC cell lines were observed by cell counting kit-8 assay, flow cytometry, and transwell assay. Xenografts mouse model was established to explore the in vivo effect of circ_0014359 on the tumor volume and size of OSCC. We found that circ_0014359 was highly expressed in the OSCC tissues and cell lines compared to the normal controls (P<0.05). The expression of circ_0014359 was associated with the survival of patients (P<0.05). For the OSCC cell lines, circ_0014359 knock down induced apoptosis and inhibited migration, invasion, and epithelial-mesenchymal transition of OSCC cells (P<0.001). In vivo, silencing the circ_0014359 blocked the growth of OSCC tumors. The circ_0014359 can directly interact with the micro-RNA-149 (miR-149). Inhibition of miR-149 can rescue the inhibitory effects of circ_0014359 knock down on OSCC cells. The circ_0014359-miR-149 pathway may be a novel target for developing strategies for the diagnosis and treatment of OSCC.

Propofol Upregulates MicroRNA-30b to Inhibit Excessive Autophagy and Apoptosis and Attenuates Ischemia/Reperfusion Injury In Vitro and in Patients.

Evidence reveals that propofol protects cells via suppressing excessive autophagy induced by hypoxia/reoxygenation (H/R). Previously, we found in a genome-wide microRNA profile analysis that several autophagy-related microRNAs were significantly altered during the process of H/R in the presence or absence of propofol posthypoxia treatment (P-PostH), but how these microRNAs work in P-PostH is still largely unknown. Here, we found that one of these microRNAs, microRNA-30b (miR-30b), in human umbilical vein endothelial cells (HUVECs) was downregulated by H/R treatment but significantly upregulated by 100 M propofol after H/R treatment. miR-30b showed similar changes in open heart surgery patients. By dual-luciferase assay, we found that Beclin-1 is the direct target of miR-30b. This conclusion was also supported by knockdown or overexpression of miR-30b. Further studies showed that miR-30b inhibited H/R-induced autophagy activation. Overexpression or knockdown of miR-30b regulated autophagy-related protein gene expression in vitro. To clarify the specific role of propofol in the inhibition of autophagy and distinguish the induction of autophagy from the damage of autophagy flux, we used bafilomycin A1. LC3-II levels were decreased in the group treated with propofol combined with bafilomycin A1 compared with the group treated with bafilomycin A1 alone after hypoxia and reoxygenation. Moreover, HUVECs transfected with Ad-mCherry-GFP-LC3b confirmed the inhibitory effect of miR-30b on autophagy flux. Finally, we found that miR-30b is able to increase the cellular viability under the H/R condition, partially mimicking the protective effect of propofol which suppressed autophagy via enhancing miR-30b and targeting Beclin-1. Therefore, we concluded that propofol upregulates miR-30b to repress excessive autophagy via targeting Beclin-1 under H/R condition. Thus, our results revealed a novel mechanism of the protective role of propofol during anesthesia. Clinical Trial Registration Number. This trial is registered with ChiCTR-IPR-14005470. The name of the trial register: Propofol Upregulates MicroRNA-30b to Repress Beclin-1 and Inhibits Excessive Autophagy and Apoptosis.

LncRNA GACAT1 targeting miRNA-149 regulates the molecular mechanism of proliferation, apoptosis and autophagy of oral squamous cell carcinoma cells.

To explore the effects of lncRNA GACAT1/miR-149 molecular axis on the proliferation, apoptosis, migration and autophagy of oral squamous cell carcinoma (OSCC) cells, and to explore its molecular mechanism. The expressions of lncRNA GACAT1 and miR-149 in tissues and cell lines of patients with OSCC were detected by qRT-PCR. Si-control, GACAT1-siRNA, inhibitor NC and miR-149 inhibitors were transfected into OSCC cells separately or in combination with Lipofectamine 2000. The binding sites between lncRNA GACAT1 and miR-149 were predicted using the miRanda website, and the targeting relationship was verified by dual-luciferase assay. The expression of lncRNA XIST and miR-149 was detected by qRT-PCR. CCK-8 assay was used to detect cell activity. Cell cycle distribution and apoptosis were detected by flow cytometry. Cell migration ability was detected by Transwell assay. The expression of migration and autophagy-related proteins was detected by western blot. LncRNA GACAT1 was highly expressed in cancer tissues and cell lines of OSCC patients (P < 0.01), while miR-149 was low expressed (P < 0.01). LncRNA GACAT1 binds to miR-149 targeting. The down-regulation of lncRNA GACAT1 inhibited the proliferation and migration of OSCC cells and promoted apoptosis and autophagy (P < 0.01). The transfection of miR-149 inhibitor had the opposite effect. Knockdown of lncRNA GACAT1 and transfection with miR-149 inhibitor reversed the effect of GACAT1 silencing on OSCC cells. Inhibition of lncRNA GACAT1 can inhibit the proliferation and migration of OSCC cells, promote apoptosis and autophagy, and the mechanism may be related to the targeting of miR-149.

Interfacial Conductivity Enhancement and Pore Confinement Conductivity-Lowering Behavior inside the Nanopores of Solid Silica-gel Nanocomposite Electrolytes.

Solid nanocomposite electrolytes (nano-SCEs) that exhibit higher ionic conductivity than the individual confined electrolyte were investigated for high-performance solid-state batteries. Understanding the behavior of Li-ion conduction through the pores is important to design ideal nanoporous structures for nano-SCEs, which are composed of an ionic liquid electrolyte (ILE) in a highly porous (∼90%) silica matrix. To establish the relationship between the pore structure of the silica matrix and the ionic conductivity of the solid nanocomposite, the liquid electrolyte fraction was successfully extracted from the nano-SCE to reveal the fragile porous silica matrix. A careful drying using the CO2 supercritical drying method helps in sustaining the original structure, preventing its collapse due to surface tension. The pore size distribution, Brunauer-Emmett-Teller (BET) surface area, and porosity were characterized using scanning electron microscopy, transmission electron microscopy, and N2 adsorption/desorption techniques. Our results revealed a wide size distribution of macropores and mesopores in the silica matrix. The pore size increased and the effective surface area decreased with increasing ILE/SiO2 molar ratio. The interface conductivity enhancement was found to increase with the thickness of the adsorbed (ice-like) bound-water layer on the silica surface, confirming that the strong hydrogen bonding of the adsorbed ionic liquid molecules on the bound-water layer causes the conduction promotion effect in the nano-SCE. In addition, a large number of small pores lead to a severe pore confinement effect that results in a decreased conductivity due to the increasing viscosity of the ILE filling the pores. The conductivity can be improved by realizing a nano-SCE with an optimized pore size to minimize the pore confinement effect.

Fast Charge Transfer across the Li7La3Zr2O12 Solid Electrolyte/LiCoO2 Cathode Interface Enabled by an Interphase-Engineered All-Thin-Film Architecture.

Lithium garnet Li7La3Zr2O12 (LLZO) is being investigated as a potential solid electrolyte for next-generation solid-state batteries owing to its high ionic conductivity and electrochemical stability against metallic lithium and high potential cathodes. While the LLZO/Li metal anode interface has been thoroughly investigated to achieve almost negligible interface resistances, the LLZO/cathode interface still suffers from high interfacial resistances mainly due to the high-temperature sintering required for proper ceramic bonding. In this work, the LLZO solid electrolyte/LiCoO2 (LCO) cathode interface is investigated in an all-thin-film model system. This architecture provides an easy access to the interface for in situ and ex situ characterization, allowing one to identify the degradation processes taking place under high-temperature cosintering and to test solutions such as interface modifications. Introducing an in situ-lithiated Nb2O5 diffusion barrier at the interface, we were able to lower the LLZO/LCO charge transfer resistance to about 50 Ω cm2, a 3-fold reduction with respect to previously reported values. The low interfacial resistance combined with the high conductance through the LLZO thin-film electrolyte allows one to investigate the charge transfer at high charge-discharge rates, unlike in bulk systems. At 1C, discharge capacities of about 140 mA h g-1 were measured, and at 10C, 60% of the theoretical capacity was retained with a cycle life over 100 cycles. Besides the role of this architecture in the interface investigation, this work also constitutes a milestone in the development of thin-film solid-state batteries with higher power densities.

Silica gel solid nanocomposite electrolytes with interfacial conductivity promotion exceeding the bulk Li-ion conductivity of the ionic liquid electrolyte filler.

The transition to solid-state Li-ion batteries will enable progress toward energy densities of 1000 W·hour/liter and beyond. Composites of a mesoporous oxide matrix filled with nonvolatile ionic liquid electrolyte fillers have been explored as a solid electrolyte option. However, the simple confinement of electrolyte solutions inside nanometer-sized pores leads to lower ion conductivity as viscosity increases. Here, we demonstrate that the Li-ion conductivity of nanocomposites consisting of a mesoporous silica monolith with an ionic liquid electrolyte filler can be several times higher than that of the pure ionic liquid electrolyte through the introduction of an interfacial ice layer. Strong adsorption and ordering of the ionic liquid molecules render them immobile and solid-like as for the interfacial ice layer itself. The dipole over the adsorbate mesophase layer results in solvation of the Li+ ions for enhanced conduction. The demonstrated principle of ion conduction enhancement can be applied to different ion systems.

Knockdown of IFI27 inhibits cell proliferation and invasion in oral squamous cell carcinoma.

BACKGROUND: The development of oral squamous cell carcinoma (OSCC) involves genetic mutations, epigenetic gene expression modification, and other processes. It has been reported that IFI27 is upregulated in OSCC, but its function is unknown. The aim of this study was to investigate the role of IFI27 on OSCC cell proliferation and invasion. METHODS: The protein level of IFI27 in OSCC tissues and adjacent tissues was detected by immunohistochemistry. In the OSCC cell model, we designed the IFI27 siRNA to downregulate the expression of IFI27; gene and protein of IFI27 in those models were then detected by Q-PCR and Western blot. MTT assay was used to detect the effect of -IFI27 knockdown on cell proliferation; Annexin V-PI staining flow cytometry was used to detect the effect of IFI27 downregulation on apoptosis of cancer cells. The effect of IFI27 downregulation on oral cancer cell invasion was detected using Transwell assay. RESULTS: IFI27 was highly expressed in OSCC tissues by immunohistochemical assay. In the OSCC cell model, IFI27 siRNA could downregulate the mRNA and protein expression level of IFI27. As showed in MTT assay, Annexin V-PI assay, and Transwell assay, through the downregulation of IFI27, TSCCA and TCA8113 cell proliferation were inhibited, OSCC cell apoptosis was promoted, and its migration and invasion were inhibited. CONCLUSION: IFI27 is involved in the development and progression of OSCC. Its high expression promotes cell proliferation and invasion and reduces apoptosis. These findings may provide new biomarkers and therapeutic targets for OSCC diagnosis and clinical treatment.

Spherical polystyrene-supported chitosan thin film of fast kinetics and high capacity for copper removal.

In order to accelerate the kinetics and improve the utilization of the surface active groups of chitosan (CS) for heavy metal ion removal, sub-micron-sized polystyrene supported chitosan thin-film was synthesized by the electrostatic assembly method. Glutaraldehyde was used as cross-linking agent. Chitosan thin-film was well coated onto the surface of the polystyrene (PS) beads characterized by scanning electron microscopy (SEM) and energy dispersive X-ray (EDX). Their adsorption toward Cu(II) ions was investigated as a function of solution pH, degree of cross-linking, equilibrium Cu(II) ions concentration and contact time. The maximum adsorptive capacity of PS-CS was 99.8 mg/g in the adsorption isotherm study. More attractively, the adsorption equilibrium was achieved in 10 min, which showed superior properties among similar adsorbents. Continuous adsorption-desorption cyclic results demonstrated that Cu(II)-loaded PS-CS can be effectively regenerated by a hydrochloric acid solution (HCl), and the regenerated composite beads could be employed for repeated use without significant capacity loss, indicating the good stability of the adsorbents. The XPS analysis confirmed that the adsorption process was due to surface complexes with atoms of chitosan. Generally, PS beads could be employed as a promising host to fabricate efficient composites that originated from chitosan or other bio-sorbents for environmental remediation.

Spherical polystyrene-supported nano-Fe3O4 of high capacity and low-field separation for arsenate removal from water.

Fe(3)O(4) is a promising material for arsenic sequestration due to its specific affinity toward arsenic and feasible magnetic separation. How to further increase its adsorption capacity while maintain its low-field separation is an interesting but challenging task. In this study nano-Fe(3)O(4) was successfully coated onto the outer surface of polystyrene (PS) beads of 350-400 nm in diameter by the hetero-coacervation method, and the resulting composite PS-Fe(3)O(4) was characterized using transmission electron microscope (TEM), X-ray powder diffraction (XRD), and electrophoresis measurement (EM). Its adsorption toward arsenate was investigated as a function of solution pH, arsenic concentration, contact time, and coexisting anions. The maximum adsorption capacity of PS-Fe(3)O(4) was 139.3mg/g Fe(3)O(4), 77.7% greater than that of bulky Fe(3)O(4). More attractively, it can be readily separated from water under a low magnetic field (<0.035 T). Continuous adsorption-desorption cyclic results demonstrated that arsenate-loaded PS-Fe(3)O(4) can be effectively regenerated by NaOH solution, and the regenerated composite beads could be employed for repeated use without significant capacity loss, indicating that nano-Fe(3)O(4) was steadily coated onto the surface of PS beads. Generally, PS beads could be employed as a promising host to fabricate efficient composites originated from Fe(3)O(4) or other nanoparticles for environmental remediation.