Crystal structure of N′ -(2, 6-dimethyl-phenyl)benzenecarboximidamide tetrahydrofuran monosolvate

Acknowledgements This work was supported by grants from the Natural Science Foundation of China (grant No. 20702029) and the Natural Science Foundation of Shanxi Province (grant No. 2008011024).Peer reviewedPublisher PD

Effect of fucoidan on B16 murine melanoma cell melanin formation and apoptosis

Background：Fucoidan is a complex sulfated polysaccharide extracted from brown seaweed and has a wide variety of biological activities. It not only inhibits cancer cell growth but also inhibits tyrosinase in vitro. Therefore, it is of interest to investigate the effect of fucoidan on B16 murine melanoma cells as the findings may provide new insights into the underlying mechanism regarding the inhibition of melanin formation by fucoidan. In the present study, we aimed to investigate the anti-melanogenic effect of fucoidan and its inhibitory effect on B16 cells.Materials and Methods: The influence of fucoidan on B16 melanoma cells and cellular tyrosinase was examined. Cell viability was examined by the cell counting kit-8 assay. Cellular tyrosinase activity and melanin content were determined using spectrophotometric methods and protein expression was analyzed by immunoblotting. Morphological changes in B16 melanoma cells were examined by phase contrast microscopy and apoptosis was analyzed by flow cytometry.Results: In vitro studies were performed using cell viability analysis and showed that fucoidan significantly decreased viable cell number in a dose-response manner with an IC50 of 550 ±4.3 μg/mL. Cell morphology was altered and significant apoptosis was induced when cells were exposed to 550 μg/mL fucoidan for 48 h.Conclusion: This study provides substantial evidence to show that fucoidan inhibits B16 melanoma cell proliferation and cellular tyrosinase activity. Fucoidan may be useful in the treatment of hyperpigmentation and as a skin-whitening agent in the cosmetics industry.Keywords: B16 melanoma cells, Fucoidan, Melanogenesis, Tyrosinas

Promoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma

<p>Abstract</p> <p>Background</p> <p>Downregulation of the putative tumor suppressor gene <it>SLC22A18 </it>has been reported in a number of human cancers. The aim of this study was to investigate the relationship between <it>SLC22A18 </it>downregulation, promoter methylation and the development and progression of human glioma.</p> <p>Method</p> <p><it>SLC22A18 </it>expression and promoter methylation was examined in human gliomas and the adjacent normal tissues. U251 glioma cells stably overexpressing <it>SLC22A18 </it>were generated to investigate the effect of <it>SLC22A18 </it>on cell growth and adherence <it>in vitro </it>using the methyl thiazole tetrazolium assay. Apoptosis was quantified using flow cytometry and the growth of <it>SLC22A18 </it>overexpressing U251 cells was measured in an <it>in viv</it>o xenograft model.</p> <p>Results</p> <p><it>SLC22A18 </it>protein expression is significantly decreased in human gliomas compared to the adjacent normal brain tissues. <it>SLC22A18 </it>protein expression is significantly lower in gliomas which recurred within six months after surgery than gliomas which did not recur within six months. <it>SLC22A18 </it>promoter methylation was detected in 50% of the gliomas, but not in the adjacent normal tissues of any patient. SLC22A18 expression was significantly decreased in gliomas with <it>SLC22A18 </it>promoter methylation, compared to gliomas without methylation. The <it>SLC22A18 </it>promoter is methylated in U251 cells and treatment with the demethylating agent 5-aza-2-deoxycytidine increased <it>SLC22A18 </it>expression and reduced cell proliferation. Stable overexpression of <it>SLC22A18 </it>inhibited growth and adherence, induced apoptosis <it>in vitro </it>and reduced <it>in vivo </it>tumor growth of U251 cells.</p> <p>Conclusion</p> <p><it>SLC22A18 </it>downregulation via promoter methylation is associated with the development and progression of glioma, suggesting that <it>SLC22A18 </it>is an important tumor suppressor in glioma.</p