Arsenic Trioxide Inhibits Cell Growth and Invasion via Down- Regulation of Skp2 in Pancreatic Cancer Cells.

Arsenic trioxide (ATO) has been found to exert anti-cancer activity in various human malignancies. However, the molecular mechanisms by which ATO inhibits tumorigenesis are not fully elucidated. In the current study, we explored the molecular basis of ATO-mediated tumor growth inhibition in pancreatic cancer cells. We used multiple approaches such as MTT assay, wound healing assay, Transwell invasion assay, annexin V-FITC, cell cycle analysis, RT-PCR and Western blotting to achieve our goal. We found that ATO treatment effectively caused cell growth inhibition, suppressed clonogenic potential and induced G2-M cell cycle arrest and apoptosis in pancreatic cancer cells. Moreover, we observed a significant down-regulation of Skp2 after treatment with ATO. Furthermore, we revealed that ATO regulated Skp2 downstream genes such as FOXO1 and p53. These findings demonstrate that inhibition of Skp2 could be a novel strategy for the treatment of pancreatic cancer by ATO.

Single-crystal-to-single-crystal transformation in a one-dimensional Ag-Eu helical system.

Single-crystal-to-single-crystal transformation of one-dimensional 4d-4f coordination polymers has been investigated for the first time. More importantly, we observed the transformation of a meso-helical chain to a rac-helical chain as a function of the temperature.

Bis[methyl 2-(2-pyridylmethyl-idene)hydrazinecarbodithio-ato]zinc(II).

In the title compound, [Zn(C(8)H(8)N(3)S(2))(2)], the Zn atom is coordinated by the two ligands in a tridentate manner, via the pyridyl N, the azomethine N and the thiol-ate S atom; the coordination geometry is distorted octa-hedral, with the two ligands in the mer configuration (two S atoms and two pyridyl N atoms are cis with respect to each other and the azomethine N atoms is trans). The mol-ecules are linked by C-H⋯S hydrogen bonds, forming a three-dimensional network structure.

[Effect of yiqi huoxue huayu recipe on vascular collagen turnover and relevant gene expression].

OBJECTIVE: To explore the effect of Yiqi Huoxue recipe (YHR), a Chinese herbal medicine for supplementing Qi, activating blood circulation to remove stasis, on vascular extracellular matrix (ECM) remodeling and its molecular mechanism. METHODS: Vascular smooth muscle cell (VSMC) proliferation activity and collagen turnover rate were detected by 3H-TdR test and hydroxyproline amount determined by 3H-Pro incorporation. Expression activity of MMP-2 and osteopontin genes was detected by Northern blotting and MMP-2 zymography analysis. RESULTS: YHR could markedly inhibit VSMC collagen synthesis stimulated by blasic fibroblast growth factor (bFGF) and lower the collagen turnover rate induced by vascular de-endothelialization. The expression level of MMP-2 and osteopontin genes was down-regulated by YHR in cultured VSMC and vascular wall with endothelial injury, and VSMC proliferation was inhibited by the serum obtained from YHR treated rats. Removing protein from the drug serum made no change on the effect of YHR to VSMC. CONCLUSION: YHR could inhibit and/or retard ECM remodeling through regulating the expression of MMP-2 and osteopontin genes and lowering the collagen turnover rate.