Arsenic Trioxide Inhibits Cell Growth and Induces Apoptosis through Inactivation of Notch Signaling Pathway in Breast Cancer

Arsenic trioxide has been reported to inhibit cell growth and induce apoptotic cell death in many human cancer cells including breast cancer. However, the precise molecular mechanisms underlying the anti-tumor activity of arsenic trioxide are still largely unknown. In the present study, we assessed the effects of arsenic trioxide on cell viability and apoptosis in breast cancer cells. For mechanistic studies, we used multiple cellular and molecular approaches such as MTT assay, apoptosis ELISA assay, gene transfection, RT-PCR, Western blotting, and invasion assays. For the first time, we found a significant reduction in cell viability in arsenic trioxide-treated cells in a dose-dependent manner, which was consistent with induction of apoptosis and also associated with down-regulation of Notch-1 and its target genes. Taken together, our findings provide evidence showing that the down-regulation of Notch-1 by arsenic trioxide could be an effective approach, to cause down-regulation of Bcl-2, and NF-κB, resulting in the inhibition of cell growth and invasion as well as induction of apoptosis. These results suggest that the anti-tumor activity of arsenic trioxide is in part mediated through a novel mechanism involving inactivation of Notch-1 and its target genes. We also suggest that arsenic trioxide could be further developed as a potential therapeutic agent for the treatment of breast cancer

Xia, J.; et al., Arsenic Trioxide Inhibits Cell Growth and Induces Apoptosis through Inactivation of Notch Signaling Pathway in Breast Cancer. Int. J. Mol. Sci. 2012, 13, 9627–9641

The authors wish to change Figure 5D of the paper published in IJMS [1]. In Figure 5D, the bands for NF-κB and Bcl-2 are similar with Notch-1 bands. The authors have carefully checked the original files and found that it is an inadvertent mistake in the published version of Figure 5D. Figure 5 is revised as follows. The authors would like to apologize for any inconvenience caused to the readers by these changes.[...

Decreased plasma levels of PDGF-BB, VEGF-A, and HIF-2α in preterm infants after ibuprofen treatment

IntroductionIbuprofen is one of the most common non-steroidal anti-inflammatory drugs used to close patent ductus arteriosus (PDA) in preterm infants. PDA is associated with bronchopulmonary dysplasia (BPD), while PDA closure by ibuprofen did not reduce the incidence of BPD or death. Previous studies have indicated an anti-angiogenesis effect of ibuprofen. This study investigated the change of angiogenic factors after ibuprofen treatment in preterm infants.MethodsPreterm infants with hemodynamically significant PDA (hsPDA) were included. After confirmed hsPDA by color doppler ultrasonography within 1 week after birth, infants received oral ibuprofen for three continuous days. Paired plasma before and after the ibuprofen treatment was collected and measured by ELISA to determine the concentrations of platelet-derived growth factor-BB (PDGF-BB) and vascular endothelial growth factor A (VEGF-A), and hypoxia-inducible factor-2α (HIF-2α).Results17 paired plasma from infants with hsPDA were collected. The concentration of PDGF-BB and VEGF-A significantly decreased after ibuprofen treatment (1,908 vs. 442 pg/mL for PDGF-BB, 379 vs. 174 pg/mL for VEGF-A). HIF-2α level showed a tendency to decrease after ibuprofen treatment, although the reduction was not statistically significant (p = 0.077).ConclusionThis study demonstrated decreased vascular growth factors after ibuprofen exposure in hsPDA infants

Symmetric universal character, integrable hierarchy, and affine Yangian of gl(1)

We define a symmetric universal character by using the affine Yangian of gl(1), which is related with a pair of 2D Young diagram which is considered as 3D Young diagrams with only one layer in z-axis direction. We also define the symmetric universal character hierarchy and prove that all symmetric universal characters are tau functions of this integrable hierarchy. Then, we construct the Boson-Fermion correspondence in the symmetric universal character hierarchy and symmetric universal character can be realized through them. Finally, the (m,n)-soliton solution of the symmetric universal character hierarchy is given by vertex operators

The Mesozoic Tectonic Transition from Compression to Extension in the South China Block: Insight from Structural Deformation of the Lushan Massif, SE China

The Lushan Massif has been considered an extensional dome which represents a typical extensional structure in South China. However, the composition and structure of the Lushan Massif are still unclear. In this study, we identified the eastern detachment fault (EDF) for the first time. In addition, many sinistral strike-slip structures have also been recognized in the Lushan area, such as the Xingzi shear zone (XZSZ) and Lianhua shear zone (LHSZ). Detailed field observation and structural analysis revealed that the former sinistral faults are tectonic boundaries of the later Lushan extensional dome (LSED). The tectonic evolution sequence was established after the structural analysis combined with zircon U-Pb dating and mica 40Ar-39Ar dating of metamorphic rocks, veins, and intrusive rocks from the strike-slip fault and detachment fault. The Lushan Massif has undergone sinistral ductile shearing within 162–150 Ma. The LSED was then formed in an extensional tectonic setting from 140 to 114 Ma. Together with the regional geological setting, we believe that the sinistral strike-slip structures, represented by the XZSZ and LHSZ, are coeval with the Tanlu fault system and could be controlled by a transpressional stress field resulting from the subduction of the Pacific Plate. The LSED was formed in a back-arc extension setting resulting from the rollback of a subducted slab. The tectonic transition from compression to extension in the South China Block took place at 150–140 Ma