miR-26b Targets CEP135 Gene to Regulate Nasopharyngeal Carcinoma Proliferation and Migration by NF-κB Pathway.

To screen microRNAs (miRNAs) and analyze their role in the nasopharyngeal carcinoma (NPC) development through differential analysis and cytological validation of the nasopharyngeal carcinoma dataset. The Gene Expression Omnibus (GEO) database of NPC-related data were utilized to screen for differential miRNAs, downstream target genes and relevant pathways, and the relationships among them were verified by luciferase reporter assay and cell co-culture. To analyze the function of miRNAs and downstream target genes, a series of mimics, inhibitors or Small interfering RNAs (siRNAs) targeting the downstream target genes were transfected into NPC cells or normal epithelial cells by cell transfection techniques. Cell Counting Kit-8 (CCK8), Transwell, Enzyme-linked immunosorbent assay (ELISA) apoptosis, and western blotting were adopted to determine the changes in cell activity, invasiveness, and apoptosis after differential miRNA and target gene overexpression or downregulation. Differential analysis of miRNA dataset showed that the expression of miR-26b was significantly downregulated in NPC, in agreement with the validation results of nasopharyngeal carcinoma cell lines. And downregulation of miR-26b expression in normal nasopharyngeal epithelial cells transformed the cells to tumors. CEP135 was identified as the miR-26b downstream target gene by mRNA dataset analysis, and a luciferase reporter test revealed a direct targeting link between the two. Upregulation of CEP135 levels in nasopharyngeal cancer cell lines increased cell activity, accelerated cell migration, and inhibited apoptosis. The Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that CEP135 exerted the above effects on cells via the NF-κB pathway, and co-culture with NF-κB pathway blockers reversed cell biological behavior to the level of the control group. MiR-26b downregulation leads to CEP135 overexpression and NF-κB pathway activation in NPC, which enhances proliferation, migration, and prevents apoptosis of nasopharyngeal carcinoma cells. Therefore, the study further clarifies the biological behavior mechanism of NPC and suggests new therapeutic options for NPC.

Boosting the Potassium-Ion Storage Performance in Soft Carbon Anodes by the Synergistic Effect of Optimized Molten Salt Medium and N/S Dual-Doping.

Soft carbon is attracting tremendous attention as a promising anode material for potassium-ion batteries (PIBs) because of its graphitizable structure and adjustable interlayer distance. Herein, nitrogen/sulfur dual-doped porous soft carbon nanosheets (NSC) have been prepared with coal tar pitch as carbon precursors in an appropriate molten salt medium. The molten salt medium and N/S dual-doping are responsible for the formation of nanosheet-like morphology, abundant microporous channels with a high surface area of 436 m2 g-1, expanded interlamellar spacing of 0.378 nm, and enormous defect-induced active sites. These structural features are crucial for boosting potassium-ion storage performance, endowing the NSC to deliver a high potassiation storage capacity of 359 mAh g-1 at 100 mA g-1 and 115 mAh g-1 at 5.0 A g-1, and retaining 92.4% capacity retention at 1.0 A g-1 after 1000 cycles. More importantly, the pre-intercalation of K atom from the molten salts helps improve the initial Coulombic efficiency to 50%, which outperforms those of the recently reported carbon anode materials with large surface areas. The density functional theory calculations further illuminate that the N/S dual-doping can facilitate the adsorption of K-ion in carbon materials and decrease the ion diffusion energy barrier during the solid-state charge migration.