PRSS3 plays an important role in the progression, metastasis and prognosis of human pancreatic cancer. Targeting the PRSS3 signalling pathway may be an effective and feasible approach for treatment of this lethal cancer.

In this work, Pd/PdO nanoparticles supported on oxidized multi-walled carbon nanotubes (OCNTs) catalyst is first time prepared by a one-pot gas-liquid interfacial plasma (GLIP) method with the precursor Pd(NO 3 ) 2 ·2H 2 O. Our results demonstrate that the presence of PdO nanoparticles can significantly enhance the catalytic performance of Pd catalyst for the reduction of 4-nitrophenol (4-NP).In this work, we demonstrate that the presence of PdO nanoparticles can significantly enhance the catalytic performance of Pd catalyst for the reduction of 4-nitrophenol (4-NP). Heterogeneous Pd/PdO nanoparticles supported on oxidized multi-walled carbon nanotubes (OCNTs) catalyst is prepared by a one-pot gas-liquid interfacial plasma (GLIP) method with the precursor Pd(NO3)22H2O. The Pd/PdO catalysts with uniform size distribution exhibit remarkable catalytic activity during the reduction of 4-NP to 4-aminophenol (4-AP) in neat water at room temperature. The turnover frequency (TOF) value is up to 750 h -1 , which shows much higher catalytic activity than single Pd nanoparticles supported on OCNTs. Our results indicate that the Pd/PdO catalyst can be readily recovered and reused for 10 times.

As a strategy for regulating entropy, thermal annealing is a commonly adopted approach for controlling dynamic pathways in colloid assembly. By coupling DNA strand-displacement circuits with DNA-functionalized colloid assembly, we developed an enthalpy-mediated strategy for achieving the same goal while working at a constant temperature. Using this tractable approach allows colloidal bonding to be programmed for synchronization with colloid assembly, thereby realizing the optimal programmability of DNA-functionalized colloids. We applied this strategy to conditionally activate colloid assembly and dynamically switch colloid identities by reconfiguring DNA molecular architectures, thereby achieving orderly structural transformations; leveraging the advantage of room-temperature assembly, we used this method to prepare a lattice of temperature-sensitive proteins and gold nanoparticles. This approach bridges two subfields: dynamic DNA nanotechnology and DNA-functionalized colloid programming.

In this study, we used MTT assays to demonstrate that a combination of SPIO-Serum and wild-type p53 overexpression can reduce ovarian cancer cell viability in vitro. Prussian blue staining and iron assays were used to determine changes in intracellular iron concentration following SPIO-Serum treatment. TEM was used to evaluate any mitochondrial damage induced by SPIO-Serum treatment, and Western blot was used to evaluate the expression of the iron transporter and lipid peroxidation regulator proteins. JC-1 was used to measure mitochondrial membrane potential, and ROS levels were estimated by flow cytometry. Finally, xCT protein expression and mitochondrial ROS levels were confirmed using fluorescence microscopy. Results: SPIO-Serum effectively induced lipid peroxidation and generated abundant toxic ROS. It also facilitated the downregulation of GPX4 and xCT, ultimately resulting in iron-dependent oxidative death. These effects could be reversed by iron chelator DFO and lipid peroxidation inhibitor Fer-1. SPIO-Serum treatment disrupted intracellular iron homeostasis by regulating iron uptake and the cells presented with missing mitochondrial cristae and ruptured outer mitochondrial membranes. Moreover, we were able to show that p53 contributed to SPIO-Serum-induced ferroptosis in ovarian cancer cells. Conclusion: SPIO-Serum induced ferroptosis and overexpressed p53 contributed to ferroptosis in ovarian cancer cells. Our data provide a theoretical basis for ferroptosis as a novel cell death phenotype induced by nanomaterials.