By co-condensation of IMes [IMes = N,N′-bis(2,6-dimethylphenyl)imidazol-2-ylidene]-bridged organosilane and bis(triethoxysilyl)ethane in the presence of template, a new mesoporous ethane−silica with a built-in bulky N-heterocyclic carbene (NHC) precursor in the framework was synthesized. N2 sorption, XRD, and TEM characterizations revealed that the synthesized material had an ordered mesostructure. FT-IR and solid state NMR investigations confirmed that the IMes moiety was covalently integrated with the solid materials. Such a functionalized material was able to coordinate Pd(OAc)2, leading to an active solid catalyst for Suzuki−Miyaura couplings of challenging aryl chlorides and benzyl chlorides under the relatively mild conditions. By using isopropyl alcohol as solvent and KO
t
Bu as base, a 78% yield for biphenyl was achieved in the presence of 0.5 mol % Pd at 80 °C within 24 h. This solid catalyst could be reused eight times without a significant decrease in activity. The high recyclability may be attributed to the functionalized, stable nanopores that efficiently prevent the in situ formed Pd nanoparticles from the aggregation into the less active large particles in the catalytic reaction. This study not only supplies a novel functionalized periodic mesoporous organosilica (PMO) but also provides an efficient solid catalyst for Suzuki−Miyaura couplings of challenging substrates.
Via a simple adsorption, the second generation Hoveyda-Grubbs catalyst was successfully immobilized on a mesoporous material SBA-1, leading to a highly recyclable solid catalyst for olefin metathesis.
Non-small-cell lung cancer (NSCLC) is the main pathological type of lung cancer and has a low overall five-year survival rate. miR-187 has been reported to play major roles in various tumor types. In this study, we explored the impact of miR-187 on NSCLC. qRT-PCR results demonstrated that miR-187 expression is lower in NSCLC and cancer cells than normal tissues and normal lung cells. miR-187 expression levels are associated with tumor size, TNM stage and overall survival rate. MTS and colony formation assays showed that high miR-187 expression inhibits NSCLC cell proliferation and colony formation ability, and flow cytometry showed that miR-187 overexpression induces cell cycle arrest at the G0/G1 phase. A luciferase reporter assay showed that FGF9 is a target of miR-187. miR-187 overexpression reduces the expression of FGF9, cyclin D1 CDK4 and CDK6. Therefore, miR-187 may present a new NSCLC treatment target by regulates cyclins-related protein expression.
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