No abstract

Summary The aim of this research was to evaluate the effects of lemon essential oil (LO, at 0.5%, 1%, 2% v/v film‐forming solutions) and surfactants (Tween 80 and Span 80 at 0.1% v/v film‐forming solutions) on physical, optical and structural properties of chitosan (CH) films. The films were formed by casting method. Results showed that the incorporation of LO provoked a decrease in water content, water vapour permeability (WVP) and mechanical properties. Less transparency and higher total colour difference were observed in CH–LO composite films. The addition of surfactants significantly increased WVP and solubility in water of CH–LO films. The film containing Tween 80 showed lower mechanical strength and higher transparency. The morphology was different depending on the LO contents and surfactant types used. Tween 80 improved the stability of LO in the film, whereas Span 80 promoted the movement of oil droplets to the film surface.

No abstract

Defects in the spindle assembly checkpoint (SAC) have been proposed to contribute to the chromosomal instability in human cancers. One of the major mechanisms underlying antimicrotubule drug (AMD) resistance involves acquired inactivation of SAC. Synuclein g (SNCG), previously identified as a breast cancer-specific gene, is highly expressed in malignant cancer cells but not in normal epithelium. Here, we show that SNCG is sufficient to induce resistance to AMD-caused apoptosis in breast cancer cells and cancer xenografts. SNCG binds to spindle checkpoint kinase BubR1 and inhibits its kinase activity. Specifically, the C-terminal (Gln106-Asp127) of SNCG binds to the N-terminal TPR (tetratricopeptidelike folds) motif of BubR1. SNCG-BubR1 interaction induces a structure change of BubR1, attenuates its interaction with other key checkpoint proteins of Cdc20, and thus compromises SAC function. SNCG expression in breast cancers from patients with a neoadjuvant clinical trial showed that SNCG-positive tumors are resistant to chemotherapy-induced apoptosis. These data show that SNCG renders AMD resistance by inhibiting BubR1 activity and attenuating SAC function. Mol Cancer Ther; 13(3); 699-713. Ó2014 AACR.