Growth inhibition and apoptotic/necrotic phenotype was observed in nanogold particle (AuNP)-treated human chronic myelogenous leukemia cells. To elucidate the underlying cellular mechanisms, proteomic techniques including two-dimensional electrophoresis/mass spectrometry and protein microarrays were utilized to study the differentially expressed proteome and phosphoproteome, respectively. Systems biology analysis of the proteomic data revealed that unfolded protein-associated endoplasmic reticulum (ER) stress response was the predominant event. Concomitant with transcriptomic analysis using mRNA expression, microarrays show ER stress response in the AuNP-treated cells. The ER stress protein markers' expression assay unveiled AuNPs as an efficient cellular ER stress elicitor. Upon ER stress, cellular responses, including reactive oxygen species increase, mitochondrial cytochrome c release, and mitochondria damage, chronologically occurred in the AuNP-treated cells. Conclusively, this study demonstrates that AuNPs cause cell death through induction of unmanageable ER stress.
Gundlach oscillation (or the standing-wave state) is a general phenomenon manifesting in the tunneling spectrum acquired from a metal surface using scanning tunneling spectroscopy. Previous studies relate the energy shift between peaks of the lowest-order Gundlach oscillation observed on the thin film and the metal substrate to the difference in their work functions. By observing Gundlach oscillations on Ag/Au(111), Ag/Cu(111), and Co/Cu(111) systems, we demonstrate that the work function difference is not the energy shift of the lowest order but the ones of higher order where a constant energy shift exhibits. Higher order Gundlach oscillations can thus be applied to determine the work function of thin metal films precisely.
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