1,018 research outputs found
Poly[2,7-(9,9-dihexylfluorene)]-block-poly[3-(trimethoxysilyl)propyl methacrylate] (PF-b-PTMSPMA) rod-coil block copolymers: Synthesis, morphology and photophysical properties in mixed solvents
No full textUsing Path analysis to examine causal relationships among balanced scorecard performance indicators for general hospitals: the case of a public hospital system in Taiwan
No full textClinical improvement following home parenteral nutrition in pediatric patients with intestinal failure.
No full textLiving Anionic Polymerization of Styrene Derivatives para-Substituted with pi-Conjugated Oligo(fluorene) Moieties
No full textYC-1 inhibits proliferation of breast cancer cells by down-regulating EZH2 expression via activation of c-Cbl and ERK
No full textBACKGROUND AND PURPOSE
YC-1 exhibits potent anticancer activity via numerous actions in many cancer cell lines. Hence, we investigated the in vivo antitumour efficacy of YC-1 in an MDA-MB-468 xenograft model and elucidated the mechanism of down-regulation of enhancer of zeste homology 2 (EZH2) by YC-1 in breast cancer cells.
EXPERIMENTAL APPROACH
In YC-1-treated breast cancer cells and tumour specimens from YC-1-treated MDA-MB-468 xenografts, EZH2 expression was analysed by Western blotting. Pharmacological inhibitors and short hairpin RNA-mediated knockdown were applied to identify possible signalling pathways involved in EZH2 down-regulation by YC-1.
KEY RESULTS
YC-1 reduced the viability of breast cancer cells and tumour growth in MDA-MB-468 xenografts. In breast cancer cells, YC-1 down-regulated EZH2 expression in a concentration-and time-dependent manner. Depletion of EZH2 reduced the proliferation and susceptibility of breast cancer cells to YC-1-induced apoptosis. EZH2 expression was suppressed in tumour specimens from YC-1-treated MDA-MB-468 xenograft mice. YC-1 enhanced both the degradation rate and ubiquitination of EZH2. The down-regulation of EZH2 by YC-1 was associated with activation of PKA and Src-Raf-ERK-mediated signalling pathways. Furthermore, depletion of Casitas B-lineage lymphoma (c-Cbl), an E3 ubiquitin ligase, abolished YC-1-induced apoptosis and suppression of EZH2. YC-1 rapidly activated c-Cbl to induce signalling associated with ERK and EZH2.
CONCLUSION AND IMPLICATIONS
We discovered that YC-1 induces apoptosis and inhibits tumour growth of breast cancer cells via down-regulation of EZH2 by activating c-Cbl and ERK. These data suggest that YC-1 is a potential anticancer drug candidate for triple-negative breast cancer
YC-1 inhibits proliferation of breast cancer cells by downregulating EZH2 expression via activation of c-Cbl and ERK
No full text[[abstract]]Background and Purpose
YC-1 exhibits potent anticancer activity via numerous actions in many cancer cell lines. Hence, we investigated the in vivo antitumour efficacy of YC-1 in an MDA-MB-468 xenograft model and elucidated the mechanism of down-regulation of enhancer of zeste homology 2 (EZH2) by YC-1 in breast cancer cells.
Experimental Approach
In YC–1-treated breast cancer cells and tumour specimens from YC–1-treated MDA-MB-468 xenografts, EZH2 expression was analysed by Western blotting. Pharmacological inhibitors and short hairpin RNA-mediated knockdown were applied to identify possible signalling pathways involved in EZH2 down-regulation by YC-1.
Key Results
YC-1 reduced the viability of breast cancer cells and tumour growth in MDA-MB-468 xenografts. In breast cancer cells, YC-1 down-regulated EZH2 expression in a concentration- and time-dependent manner. Depletion of EZH2 reduced the proliferation and susceptibility of breast cancer cells to YC–1-induced apoptosis. EZH2 expression was suppressed in tumour specimens from YC–1-treated MDA-MB-468 xenograft mice. YC-1 enhanced both the degradation rate and ubiquitination of EZH2. The down-regulation of EZH2 by YC-1 was associated with activation of PKA and Src–Raf–ERK-mediated signalling pathways. Furthermore, depletion of Casitas B-lineage lymphoma (c-Cbl), an E3 ubiquitin ligase, abolished YC–1-induced apoptosis and suppression of EZH2. YC-1 rapidly activated c-Cbl to induce signalling associated with ERK and EZH2.
Conclusion and Implications
We discovered that YC-1 induces apoptosis and inhibits tumour growth of breast cancer cells via down-regulation of EZH2 by activating c-Cbl and ERK. These data suggest that YC-1 is a potential anticancer drug candidate for triple-negative breast cancer
Synthesis and characterization of fluorinated beta-ketoiminate and imino-alcoholate Pd complexes: precursors for palladium chemical vapor deposition
Full text link[[abstract]]The design and synthesis of Pd complexes with two beta-ketoiminate or with two imino-alcoholate chelate ligands is reported. In order to establish their structures in the solid-state, methoxyethyl substituted complexes 1c and 2c were characterized by single crystal X-ray diffraction, showing a square-planar local coordination for the Pd atom, but the beta-ketoiminate ligands of 1c gave a bent basal plane involving two chelating hexagons, which was in sharp contrast to the boat configuration of the imino-alcoholate ligands observed in the second complex 2c. Chemical vapor deposition (CVD) experiments were conducted at deposition temperatures of 250-350 degreesC. Scanning electron micrographs (SEM) were taken to reveal the surface morphologies and grain sizes of the Pd metal thin films. The resulting thin films were found to contain a low level of carbon and oxygen impurities using O-2 as the carrier gas, as measured by X-ray photoelectron spectroscopy (XPS).[[fileno]]2010302010012[[department]]化學
Citrus peel extracts attenuated obesity and modulated gut microbiota in mice with high-fat diet-induced obesity
No full text[[abstract]]Polymethoxyflavones (PMFs) and hydroxyl PMFs (HOPMFs) are mainly found in citrus peel and have shown anti-obesity potential in in vitro and in vivo studies. Herein, we have investigated the anti-obesity effects of two citrus peel extracts obtained via supercritical fluid extraction: PMF A, with a lower content of PMFs and HOPMFs, and PMF B, with a higher content of PMFs and HOPMFs. PMF A and PMF B were administered orally for 16 weeks to mice with high fat diet (HFD)-induced obesity. The results showed that PMF B decreased the lipid content more statistically significantly (p < 0.05) than PMF A in 3T3-L1 preadipocytes, reduced the adipocyte size, decreased the adipose tissue weight and alleviated the total body weight in the HFD mice. Both PMF A and PMF B reduced the adipocyte size in the perigonadal fat by markedly decreasing the levels of lipid droplets (LD) and perilipin 1 protein and Sterol regulatory element binding protein 1 (SREBP-1) expression. Compared to the case of the HFD group, PMF B altered the gut microbiota by increasing Prevotella and decreasing rc4-4 bacteria. The change in the composition of gut microbiota, the community of symbiotic and pathogenic microorganisms, may determine the metabolic health and be responsible for the anti-obesity mechanism. Our results indicate that the citrus peel extracts decrease lipid accumulation both in vivo and in vitro and should be considered for the management of overweight and obesity conditions
Clinical Outcomes of Dialysis Patients Treated with Drug-Eluting Stent for Left Main Distal Bifurcation Lesions
No full textAims: We assessed clinical outcomes after percutaneous coronary intervention (PCI) for unprotected left main coronary artery (ULMCA) distal bifurcation lesions using drug-eluting stents (DES) in hemodialysis (HD) patients compared to non-HD patients. Methods and Results: We identified 1,858 consecutive patients who underwent PCI for ULMCA distal bifurcation lesions at 4 high-volume centers in Japan, Italy, and Taiwan between January 2005 and December 2015. Of them, 1,416 patients were treated with DES including 113 HD patients and 1,303 non-HD patients. The primary end point was target lesion failure (TLF) defined as a composite of cardiac death, target lesion revascularization (TLR), and myocardial infarction. HD patients were more likely to be younger and have diabetes mellitus, dyslipidemia, peripheral artery disease, lower ejection fraction, and higher EuroSCORE. TLF rate at 3 years was significantly higher in HD group than in non-HD group (adjusted hazard ratio [HR] 2.43 [1.75-3.38], p < 0.001). Cardiac mortality and TLR rate were also significantly higher in HD group than in non-HD group (adjusted HR 3.85 [2.34-6.34], p < 0.001, and HR 2.10 [1.41-3.14], p < 0.001, respectively). Conclusions: HD was strongly associated with adverse cardiac events after PCI for ULMCA distal bifurcation lesions with DES
YC-1 enhances the anti-tumor activity of sorafenib through inhibition of signal transducer and activator of transcription 3 (STAT3) in hepatocellular carcinoma
Full text linkBackground: Traditional systemic chemotherapy does not provide survival benefits in patients with hepatocellular carcinoma (HCC). Molecular targeted therapy shows promise for HCC treatment, however, the duration of effectiveness for targeted therapies is finite and combination therapies offer the potential for improved effectiveness. Methods: Sorafenib, a multikinase inhibitor, and YC-1, a soluble guanylyl cyclase (sGC) activator, were tested in HCC by proliferation assay, cell cycle analysis and western blot in vitro and orthotopic and ectopic HCC models in vivo. Results: In vitro, combination of sorafenib and YC-1 synergistically inhibited proliferation and colony formation of HepG2, BEL-7402 and HCCLM3 cells. The combination also induced S cell cycle arrest and apoptosis, as observed by activated PARP and caspase 8. Sorafenib and YC-1 respectively suppressed the expression of phosphorylated STAT3 (p-STAT3) (Y705) in a dose-and time-dependent manner. Combination of sorafenib and YC-1 significantly inhibited the expression of p-STAT3 (Y705) (S727), p-ERK1/2, cyclin D1 and survivin and SHP-1 activity compared with sorafenib or YC-1 used alone in all tested HCC cell lines. In vivo, sorafenib-YC-1 combination significantly suppressed the growth of HepG2 tumor xenografts with decreased cell proliferation and increased apoptosis observed by PCNA and PARP. Similar results were also confirmed in a HCCLM3 orthotopic model. There was a reduction in CD31-positive blood vessels and reduced VEGF expression, which suggested a combinational effect of sorafenib and YC-1 on angiogenesis. The reduced expression of p-STAT3, cyclin D1 and survivin was also observed with the combination of sorafenib and YC-1. Conclusions: Our data show that sorafenib-YC-1 combination is a novel potent therapeutic agent that can target the STAT3 signaling pathway to inhibit HCC tumor growth.Biochemistry & Molecular BiologyOncologySCI(E)[email protected]; [email protected]
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