Characterization of an Iron-Copper Bimetallic Metal-Organic Framework for Adsorption of Methyl Orange in Aqueous Solution.

Iron-based organic frame material MIL-53 (Fe) was synthesized by the hydrothermal method with Cu2+ incorporated to obtain bimetallic composite MIL-53 (Fe, Cu). The structure and morphology of the material were characterized by SEM, XRD, BET, FTIR, XPS, and zeta potential. The adsorption performance of MIL-53 (Fe, Cu) on methyl orange was tested under a variety of conditions, including the effects of pH and material dosage, by the static adsorption test. The results show that under the condition of pH = 7, a temperature of 30°C, and an adsorbent dosage of 20 mg, the removal rate of MIL-53 (Fe, Cu) for methyl orange can reach more than 96% within 4 h, and the maximum adsorption capacity after fitting by the thermodynamic model can reach 294.43 mg/g, showing the excellent adsorption performance of MIL-53 (Fe, Cu) on methyl orange. In addition, by exploring the adsorption mechanism of MIL-53 (Fe, Cu) on methyl orange, it is found that the adsorption of MIL-53 (Fe, Cu) on methyl orange depends on chemical adsorption, as evidenced by combining Fe3+ and Cu2+ in the material with methyl orange molecules to form complexes to achieve adsorption. While the specific surface area of the material had no obvious effect on adsorption, the effects of pH, temperature, and concentration were explored. At a pH of 6.5, greater adsorption occurred at higher temperatures, as determined by thermodynamic model fitting, as well as with higher initial methyl orange molecule concentration.

Proliferation and migration mediated by Dkk-1/Wnt/beta-catenin cascade in a model of hepatocellular carcinoma cells.

Beta-catenin is a multifunctional protein acting as a key factor in the cadherin-mediated cell-cell adhesion system and in the Wnt signaling pathway. To demonstrate the molecular mechanisms of metastasis of hepatocellular carcinoma (HCC) cells, we established a metastatic subclone of human HCC H7402 cells, termed M-H7402, by isolating from transplantation of H7402 cells into severe combined immunodeficient (SCID) mice. Based on the 2 parallel cell lines, we investigated the roles of dickkopf-1 (Dkk-1) and Wnt/beta-catenin pathway in proliferation and migration of HCC cells. cDNA microarray showed that 24 genes were related to tumor metastasis differentially expressed between H7402 and M-H7402 cells. Western blot analysis revealed that the expression levels of beta-catenin, c-Myc, and cyclin D1 were upregulated, but Dkk-1 and nm23 were dramatically downregulated in M-H7402 cells, which suggests that the 2 cell lines were remarkably different in molecular events associated with metastasis. Furthermore, we found that overexpression of Dkk-1 by transfection was able to downregulate the expression of c-Myc and cyclin D1, and it also inhibited the growth and migration in M-H7402 cells. Although reduction of Dkk-1 expression by RNA interference was able to upregulate the expression of beta-catenin, c-Myc, and cyclin D1 in H7402 cells, it also promoted beta-catenin translocation from cytoplasm into nuclei and increased the migration of the cells. Therefore, we conclude that Dkk-1/Wnt/beta-catenin cascade may mediate the proliferation and migration of HCC cells during the metastasis process.