Oxygen vacancy-rich porous Co 3 O 4 nanosheets (OV-Co 3 O 4 ) with diverse surface oxygen vacancy contents were synthesized via facile surface reduction and applied to NO reduction by CO and CO oxidation. The structure−activity relationship between surface oxygen vacancies and catalytic performance was systematically investigated. By combining Raman, X-ray diffraction, transmission electron microscopy, X-ray photoelectron spectroscopy, and O 2 -temperature programmed desorption, it was found that the efficient surface reduction leads to the presence of more surface oxygen vacancies and thus distinctly enhance the surface oxygen amount and mobility of OV-Co 3 O 4 . The electron transfer towards Co sites was promoted by surface oxygen vacancies with higher content. Compared with the pristine porous Co 3 O 4 nanosheets, the presence of more surface oxygen vacancies is beneficial for the catalytic performance enhancement for NO reduction by CO and CO oxidation. The OV-Co 3 O 4 obtained in 0.05 mol L −1 NaBH 4 solution (Co 3 O 4 -0.05) exhibited the best catalytic activity, achieving 100% NO conversion at 175 °C in NO reduction by CO and 100% CO conversion at 100 °C in CO oxidation, respectively. Co 3 O 4 -0.05 exhibited outstanding catalytic stability and resistance to high gas hour space velocity in both reactions. Combining in situ DRIFTS results, the enhanced performance of OV-Co 3 O 4 for NO reduction by CO should be attributed to the promoted formation and transformation of dinitrosyl species and −NCO species at lower and higher temperatures. The enhanced performance of OV-Co 3 O 4 for CO oxidation is due to the promotion of oxygen activation ability, surface oxygen mobility, as well as the enhanced CO 2 desorption ability. The results indicate that the direct regulation of surface oxygen vacancies could be an efficient way to evidently enhance the catalytic performance for NO reduction by CO and CO oxidation.

Aim: Silibinin is known to exert growth inhibition and cell death together with cell cycle arrest and apoptosis in human prostate cancer cells. Whether silibinin could inhibit the invasion, motility and migration of prostate cancer cells remains largely unknown. This study was designed to evaluate this efficacy and possible mechanisms using a novel highly bone metastatic ARCaP M cell model. Methods: Four prostate cancer cell lines, LNCaP, PC-3, DU145, and ARCaP M , were used in this study. These cells were treated with increasing concentrations of silibinin (50, 100, and 200 μmol/L) for different periods of time. After treatment, cell viabilities of four prostate cancer cells were compared by MTT assay. Alterations of ARCaP M cell invasion, motility and migration were assessed by cell invasion, motility and wound healing assays. The changes of vimentin expression were observed by Western blotting and immunofluorescence staining, and the expression of MMP-2, MMP-9, and uPA was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). Results: ARCaP M cells showed less sensitivity to the growth inhibition of pharmacological doses of silibinin than LNCaP, PC-3, and DU145 cells. However, silibinin exerted significant dose-and time-dependent inhibitory effects on the invasion, motility and migration of ARCaP M cells. Furthermore, the expression of vimentin and MMP-2, but not MMP-9 or uPA, was down-regulated in a dose-and timedependent manner after treatment of silibinin. Conclusion: This study shows that silibinin could inhibit the invasion, motility and migration of ARCaP M cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis.

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Aim: The aim of the present study was to investigate whether low dose genistein affects the invasion and epithelial mesenchymal transition (EMT) of prostate cancer (PCa) cells. Methods: Human PCa cell lines, IA8-ARCaP and LNCaP/ HIF-1a, were used in this study. The cell lines were found to process EMT in our previous study. The PCa cells were treated with increasing concentrations, from 0.1 to 75 µmol/L. Proliferation was assessed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. EMT was proven by cell morphological transition and the expression changes of EMT-related markers, which were confirmed by RT-PCR, Western blotting, and indirect immunofluorescence labeling. Transwell invasion assay was used to analyze the invasive potency. Results: The addition of genistein to the medium reduced the IA8-ARCaP and LNCaP/HIF-1a viable cell number in a dose-dependent manner (with increasing concentrations from 15 to 75 µmol/L). Less than 15 µmol/L genistein was selected as the low dose concentration, which did not affect cell proliferation. The treatment of cells with low-dose genistein induced the reversal of EMT, which was confirmed by cell morphological transition and the expression changes of EMT-related markers. The reversal of EMT in the PCa cells by low-dose genistein was in a dose-dependent manner. Moreover, low-dose genistein effectively inhibited invasion of the PCa cells in vitro. Conclusion: These results showed that treatment with low-dose genistein may be a potential strategy for the suppression of invasive growth through the reversal of EMT in cancer cells, which justifies the potential use of soybean foods as a practical chemopreventive approach for patients with PCa.

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