An aggregation or assembly of Ag triangular nanoplates (Ag TNPs) can cause dramatic changes in their optical properties, which is widely used in applications in the field of sensing. The assembly forms of nanoparticles are crucial for obtaining sensitive sensing signals, but it is unknown what kind of assembly dominates the aggregated Ag TNPs in aqueous solutions. Herein, using thiram-induced Ag TNP aggregation as a model, six different assembly models were established, including three planar (side-by-side, side-to-tip, and tip-to-tip) assemblies and three tridimensional (plane-to-plane, plane-to-tip, and plane-to-side) assemblies. The corresponding optical properties were then investigated. Both theoretical and experimental findings indicate that three-dimensional assemblies, especially plane-to-plane assembly, dominate the Ag TNPs aggregation solution, causing a blue shift of the absorption spectrum. Analysis of charge distribution patterns in Ag TNPs indicates that such a blue shift is caused by the electrostatic repulsive force in plane-to-plane assembly. Thus, we propose a simple colorimetric method for thiram detection using Ag TNPs as an indicator. The method exhibits a selective and sensitive response to thiram with a limit of detection of 0.13 μM in the range of 0.2–0.5 μM, as well as excellent performance in real samples like wheat.
Thyroid Cancer (TC) is the most common malignant tumor of the endocrine system. Cystatin M/E (CST6) has been demonstrated to have a multifaceted role in several types of cancers. However, its potential mechanisms in the progression of TC have not been fully identified. Our results revealed that CST6 expressions were upregulated in TC tissues and cells compared with normal thyroid tissues and cells. High expression of CST6 was negatively correlated with poor prognosis of thyroid cancer patients. Functional assays showed that CST6 promoted TC cells malignant phenotype, including proliferation, colony formation, migration, and invasion. Inhibition of CST6 remarkably alleviated tumor growth and metastasis of ATC xenografts in nude mouse and zebrafish model. CST6 showed interaction with cathepsin B (CTSB). CTSB knockdown profoundly inhibited the aggressive behavior of TC cells. Of note, loss of CST6 attenuated the activity of CTSB, which led to the decrease of autophagy progress. Collectively, our findings demonstrated an essential role of CST6 in the development of TC through CTSB-mediated autophagy.
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