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Arsenic trioxide has been proven to trigger apoptosis in human hepatocellular carcinoma cells. Endoplasmic reticulum stress has been known to be involved in apoptosis through the induction of CCAAT/enhancer-binding protein homologous protein. However, it is unknown whether endoplasmic reticulum stress mediates arsenic trioxide-induced apoptosis in human hepatocellular carcinoma cells. Our data showed that arsenic trioxide significantly induced apoptosis in human hepatocellular carcinoma cells. Furthermore, arsenic trioxide triggered endoplasmic reticulum stress, as indicated by endoplasmic reticulum dilation, upregulation of glucose-regulated protein 78 and CCAAT/enhancer-binding protein homologous protein. We further found that 4-phenylbutyric acid, an inhibitor of endoplasmic reticulum stress, alleviated arsenic trioxide-induced expression of CCAAT/enhancer-binding protein homologous protein. More important, knockdown of CCAAT/enhancer-binding protein homologous protein by siRNA or inhibition of endoplasmic reticulum stress by 4-phenylbutyric acid alleviated apoptosis induced by arsenic trioxide. Consequently, our results suggested that arsenic trioxide could induce endoplasmic reticulum stress-mediated apoptosis in hepatocellular carcinoma cells, and that CCAAT/enhancer-binding protein homologous protein might play an important role in this process. [ABSTRACT FROM AUTHOR]

Abstract Transition metal silicide nanowires exhibit low resistivity, great thermal stability and excellent mechanical strength, contributing to their applications as interconnection and contact materials for future integrated circuits devices. In this work, we successfully fabricated two kinds of chromium silicide/silicon heterostructure nanowires through solid state reactions — bare Si/Cr 3 Si nanowires and Si/Cr 5 Si 3 -Al 2 O 3 core-shell nanowires. The growth behaviors and diffusion mechanisms of the two silicide heterostructure nanowires were investigated with in-situ TEM at 700 °C. During the growth of chromium silicide nanowires, unique amorphous Si phase would form first in front of silicide nanowires. Also, we found that oxide-shell could control the diffusion process in silicon nanowires. With oxide-shell, compression stress would restrain the growth of chromium silicide in the radial direction but accelerate its growth rate in the axial direction. Additionally, Al 2 O 3 shell reduced the radial expansion of chromium silicide nanowires and hindered Cr-rich phases with Cr 5 Si 3 appearing as the first phase. The crystal structures of the nanowires have been identified to be single-crystalline A15 and D8m type structure of the intrinsic Cr 3 Si nanowires and Cr 5 Si 3 nanowires, respectively. In addition to fundamental science, the significant study is beneficial for future processing techniques in nanotechnology and related applications. Graphical abstract With in-situ transmission electron microscopy (TEM), we successfully transformed single crystalline Si nanowires to chromium silicide/Si nanowire heterostructures. Also, during the solid state phase transformation process, we observed unique structures at the interface, demonstrated to be amorphous Si phase after Si Si bond breaking, which led the chromium silicide nanowire growth by interface-reaction control. Unlabelled Image Highlights • We utilized solid state reactions to fabricate controllable and unique Cr 3 Si/Si and Cr 5 Si/Si nanowire heterostructures. • With in-situ transmission electron microscopy (TEM), we observed a special interfacial reaction during the silicidation. • The design of Si-Al 2 O 3 core-shell effectively improved the morphology and crystallinity of the nanowire heterostructures. • We used distinctive methods and results to systematically investigate the kinetics of the nanowire heterostructures. [ABSTRACT FROM AUTHOR]