ABSTRACT
In this study, a tungstated zirconia (WOx/ZrO2) catalyst was developed for the continuous synthesis of adiponitrile (ADN) by gas-phase nitrilation of dimethyl adipate (DMA) with NH3. The highest TOFADN could be reached on WOx/ZrO2 bearing â¼1D WOx species (highly dispersed and discontinuous status) at the surface, which, however, delivered the poorest selectivity toward nitrilation (SADN+MCP). In comparison, both efficient and selective transformation of DMA to ADN was achieved by fabricating WOx/ZrO2 with continuously distributed oligomeric WOx species (â¼2D) at the surface, either by varying the dosage of the W-reagent in the preparation of WOx(m)/ZrO2 or by doping a proper amount of the Mn element into WOx(5.0)/ZrO2, bearing WO3 NPs. Furthermore, the in situ diffuse reflectance infrared Fourier transform spectroscopy investigations of both independent and competitive adsorptions of ester functionality and NH3 over W-O-Zr, W-O-W, and Zr-O-Zr boundaries at the surface clarified the synergistic effect of these species in the activation of DMA/NH3 and thereby nitrilation.
ABSTRACT
Electroreduction of CO2 on a polymer-modified Cu-based catalyst has shown high multi-electron reduction (>2 e- ) selectivity, however, most of the corresponding current densities are still too small to support industrial applications. In this work, we designed a poly(ionic liquid) (PIL)-based Cu0 -CuI tandem catalyst for the production of C2+ products with both high reaction rate and high selectivity. Remarkably, a high C2+ faradaic efficiency (FE C 2 + ) of 76.1 % with a high partial current density of 304.2â mA cm-2 is obtained. Mechanistic studies reveal the numbers and highly dispersed Cu0 -PIL-CuI interfaces are vital for such reactivity. Specifically, Cu nanoparticles derived Cu0 -PIL interfaces account for high current density and a moderate C2+ selectivity, whereas CuI species derived PIL-CuI interfaces exhibit high activity for C-C coupling with the local enriched *CO intermediate. Furthermore, the presence of the PIL layer promotes the C2+ selectivity by lowering the barrier of C-C coupling.
ABSTRACT
PURPOSE: Keratin 18 (KRT18) is a cytoskeleton protein that plays a key role in multiple cancers. The present study aims to further investigate the roles of KRT18 in gastric cancer (GC) tissues and cells. METHODS: The KRT18 protein expression levels of GC tissues and cells were detected using immunohistochemistry and western blot. The relationship between KRT18 expression levels and the prognosis of GC patients was further analyzed. To explore this relationship, small interfering RNA (siRNA) was used to inhibit the endogenous expression of KRT18 in GC cells. Furthermore, the effects of KRT18 on the proliferation, invasion, migration, and apoptosis of GC cells were analyzed in vitro. In addition, the role of KRT18 in GC-specific processes was investigated. RESULTS: Keratin 18 expression was shown to be up-regulated in GC tissues and associated with poor prognosis. Following KRT18 silencing with siRNA, the proliferation, invasion, and migration ability of GC cells were significantly inhibited, while the apoptotic process was promoted. Furthermore, the activation of the MAPK signalling pathway was identified as the potential mechanism through which KRT18 influenced GC processes. CONCLUSIONS: Keratin 18 plays a cancer-promoting role and might be a potential therapeutic target in the treatment of GC.
ABSTRACT
In this study, the covalent bonding of linear poly(ionic liquid)s (PILs) with covalent organic frameworks (COFs) was accessed by copolymerization of a vinyl-decorated COF with 4-vinylbenzyl chloride, followed by quaternization with tertiary amines. The resultant PIL-COF composite by anchoring a proper content of vinyl sites on the COF-based comonomer retains the crystallinity and porosity, thereby facilitating access of the reactants to the catalytic active sites. As a proof of concept, the dehydrative transformation of sorbitol into isosorbide was selected as a benchmark reaction, whose rate improved significantly in the presence of PIL-COF-0.33 compared with those of individual components and the mesoporous PIL counterpart due to uniform pore sizes and flexible linear catalytic chains. In addition, the hybrids bearing a chemical cross-linkage between PILs and COFs are robust, and PIL-COF-0.33 can be recovered and reused for 10 runs without significant reactivity loss. These findings provide the basis for a novel design concept for achieving both efficient and stable IL catalysis.
ABSTRACT
The present study aimed to examine the association between hypoxia-inducible factor (HIF)-1α and the Wnt/ß-catenin signaling pathway in a hypoxic environment. The study also aimed to explore the possible mechanisms underlying the invasion of hypoxic gastric cancer cells in vitro and in vivo. The pcDNA™ 6.2GW/EmGFPmiRßcatenin plasmid was transfected into SGC7901 gastric cancer cells, resulting in cells with stable suppression of ßcatenin expression. The biological characteristics of the control, liposome, negative control, ßcatenin knockdown, hypoxia and hypoxia ßcatenin knockdown groups were tested using an invasion assay. The differences in the invasive capacity of the control, negative control and liposome groups were not statistically significant. However, the hypoxia group demonstrated a significantly enhanced invasive capacity, as compared with that in the control group (P<0.05). In the hypoxia ßcatenin knockdown group, reduced cell penetration and diminished invasive behavior was observed (P<0.05). In the hypoxia and double (chemical + physical) hypoxia groups, HIF1α, ßcatenin, urokinasetype plasminogen activator (uPA) and matrix metalloproteinase (MMP7) protein and mRNA expression levels were elevated. In response to knockdown of ßcatenin expression, HIF1α, ßcatenin, uPA and MMP7 protein as well as mRNA expression levels were significantly reduced in the hypoxia ßcatenin knockdown and the double hypoxia ßcatenin knockdown groups. In an in vivo experiment, the growth rate of xenograft tumors of hypoxic and control cells was high alongside increased HIF1α, ßcatenin, uPA and MMP7 levels according to western blot and immunohistochemical analyses, while growth and protein levels of tumors from hypoxic ßcatenin knockdown cells were significantly lower and those of ßcatenin knockdown cells were lowest. In conclusion, these results suggested that HIF1α activation was able to regulate the Wnt/ßcatenin pathway, and that HIF1α may be controlled by the Wnt/ßcatenin pathway. A potential mechanism underlying SGC7901 tumorigenicity is the activation of the Wnt/ßcatenin signaling pathway, which activates uPA and MMP7 expression and contributes to the enhanced invasion of hypoxic cancer cells.