Targeted Knockdown of Macrophage Migration Inhibitory Factor Enhances UVB Irradiation-Induced Apoptosis Via Increasing ROS Generation in Oral Squamous Cell Carcinoma.

Objectives: We investigated the effects of macrophage migration inhibitory factor (MIF) knockdown or overexpression combined with ultraviolet radiation B (UVB) irradiation on cell proliferation and apoptosis of oral squamous cell carcinoma (OSCC). Methods: MIF expression in OSCC and adjacent tissues was detected by immunohistochemistry. MIF expression in human immortalized oral epithelial cells (HIOEC) and OSCC cells was detected by western blotting. MIF was knocked down or overexpressed in OSCC cell lines (SCC-25 and CAL-27). OSCC cells were set up into control (CON), MIF overexpression/knockdown (oeMIF/shMIF), CON + UVB, and oeMIF + UVB/shMIF + UVB groups based on their exposure to UVB irradiation. Cell line proliferation was studied using a cell counting kit-8 (CCK-8) and colony formation assays. Flow cytometry was applied for determination of apoptosis, cell cycle, reactive oxygen species (ROS) abundance, and mitochondrial membrane potential. Apoptosis-related proteins were assayed by western blotting. Results: The expression of MIF was significantly higher in OSCC tissues and cell lines than in adjacent tissues and HIOEC. MIF knockdown accompanied by UVB irradiation significantly hampered cell viability and proliferation compared to MIF knockdown or UVB irradiation alone. Western blotting and flow cytometry showed that MIF knockdown combined with UVB irradiation not only induced apoptosis via the mitochondrial pathway but also mediated the cell cycle. Flow cytometry showed that ROS and mitochondrial membrane potential depolarization were increased in the combination treatment groups compared with the mono-treatment groups. Additionally, the ROS scavenger N-acetylcysteine significantly attenuated MIF knockdown combined with UVB irradiation-induced apoptosis and reversed MIF knockdown combined with UVB irradiation-induced MAPK activation. Conclusion: MIF knockdown combined with UVB irradiation significantly inhibited the proliferation of OSCC cells. MIF was involved in UVB-induced ROS generation and enhanced UVB irradiation-induced mitochondria-dependent apoptosis of OSCC cells by activating the MAPK pathway. This suggests that MIF-targeted therapy combined with UVB irradiation may be a novel approach for treating OSCC.

Enhanced piezoelectric effect at the edges of stepped molybdenum disulfide nanosheets.

The development of piezoelectric layered materials may be one of the key elements enabling expansion of nanotechnology, as they offer a solution for the construction of efficient transducers for a wide range of applications, including self-powered devices. Here, we investigate the piezoelectric effect in multilayer (ML) stepped MoS2 flakes obtained by liquid-phase exfoliation, which is especially interesting because it may allow the scalable fabrication of electronic devices using large area deposition techniques (e.g. solution casting, spray coating, inkjet printing). By using a conductive atomic force microscope we map the piezoelectricity of the MoS2 flakes at the nanoscale. Our experiments demonstrate the presence of electrical current densities above 100 A cm-2 when the flakes are strained in the absence of bias, and the current increases proportional to the bias. Simultaneously collected topographic and current maps demonstrate that the edges of stepped ML MoS2 flakes promote the piezoelectric effect, where the largest currents are observed. Density functional theory calculations are consistent with the ring-like piezoelectric potential generated when the flakes are strained, as well as the enhanced piezoelectric effect at edges. Our results pave the way to the design of piezoelectric devices using layered materials.

Restructuring and remodeling of NaREF4 nanocrystals by electron irradiation.

NaREF4 nanocrystals are found to be highly manipulable by electron beam irradiation. With 200 kV electron beam irradiation, both 14.6 nm spherical NaGdF4 :Yb,Er nanoparticles and 44.7 nm × 34.1 nm ellipsoidal NaYF4 :Yb,Er nanorods form hollow structures and eventually convert to the corresponding REF3 upon prolonged irradiation. Furthermore, the NaYF4 nanorods fractured with irradiation with a 100 kV electron source are found to be subsequently self-healed when irradiated with a 200 kV source. The detailed experimental results, in combination with theoretical analysis, suggest that knock-on effects, specific lattice energy, and the inherently low surface energy of NaREF4 collectively contribute to the formation of the hollow structures. These mechanisms allow controlled engineering and manipulation of RE nanomaterials on the nanometer scale.