Prostate cancer lineage plasticity is a key driver in the transition to neuroendocrine prostate cancer (NEPC), and the RTK/RAS signaling pathway is a well-established cancer pathway. Nevertheless, the comprehensive link between the RTK/RAS signaling pathway and lineage plasticity has received limited investigation. In particular, the intricate regulatory network governing the interplay between RTK/RAS and lineage plasticity remains largely unexplored. The multi-omics data were clustered with the coefficient of argument and neighbor joining algorithm. Subsequently, the clustered results were analyzed utilizing the GSEA, gene sets related to stemness, multi-lineage state datasets, and canonical cancer pathway gene sets. Finally, a comprehensive exploration of the data based on the ssGSEA, WGCNA, GSEA, VIPER, prostate cancer scRNA-seq data, and the GPSAdb database was conducted. Among the six modules in the clustering results, there are 300 overlapping genes, including 3 previously unreported prostate cancer genes that were validated to be upregulated in prostate cancer through RT-qPCR. Function Module 6 shows a positive correlation with prostate cancer cell stemness, multi-lineage states, and the RTK/RAS signaling pathway. Additionally, the 19 leading-edge genes of the RTK/RAS signaling pathway promote prostate cancer lineage plasticity through a complex network of transcriptional regulation and copy number variations. In the transcriptional regulation network, TP63 and FOXO1 act as suppressors of prostate cancer lineage plasticity, whereas RORC exerts a promoting effect. This study provides a comprehensive perspective on the role of the RTK/RAS pathway in prostate cancer lineage plasticity and offers new clues for the treatment of NEPC.

Surface plasmon resonance sensors relying on conventional metals such as gold and silver are plagued by problems including low hardness, vulnerability to defects, and high costs. In this research, a Kretschmann-configuration long-range surface plasmon resonance sensor is ingeniously designed by leveraging black phosphorus (BP). As a two-dimensional material, BP possesses a thickness-tunable direct bandgap, which facilitates efficient excitation of surface plasmon polaritons. The sensor architecture comprises a prism, a coupling dielectric layer, a BP film, and a sensing medium. Through meticulous optimization of parameters like the BP layer number (set to 7), the thickness of the coupling dielectric layer (optimized to 850 nm), and the refractive index, the sensor achieves an impressive sensitivity of 63.71 °/RIU and a figure of merit of 303.38 /RIU when an N-BK7 prism is utilized. In comparison to sensors based on materials such as graphene, Ag, and Au, this BP-based sensor demonstrates a superior equilibrium between sensitivity and the sharpness of the resonance spectrum. This superiority is corroborated by the analysis of the electric field distribution.

JOURNAL/mgres/04.03/01612956-202701000-00001/figure1/v/2026-11-03T121139Z/r/image-tiff Reactive oxygen species act as essential mediators in physiological processes, yet excess reactive oxygen species cause cellular damage and inflammation. Current strategies for reactive oxygen species monitoring and intervention remain limited in clinical practice. Here, we report selenium quantum dots (SeQDs) coated with peach gum (PG@SeQDs), a fluorescent nanocomposite for simultaneous reactive oxygen species detection and scavenging. SeQDs serve as fluorescent emitters and reactive oxygen species-active centers encapsulated by peach gum as a stabilizing matrix. Transmission electron microscopy and dynamic light scattering show SeQDs ~5 nm (hydrodynamic ~47 nm) and PG@SeQDs ~170 nm (hydrodynamic ~204 nm), with a zeta potential shift from –2.1 to –7.4 mV after peach gum coating, indicating enhanced colloidal stability. PG@SeQDs exhibit excitation-dependent emission, with a maximum intensity near 260 nm. Biocompatibility assays in Schwann cells show markedly higher viability for PG@SeQDs versus SeQDs and minimal hemolysis (0.24–0.32%). Antioxidant activity by 1,1-diphenyl-2-picrylhydrazyl shows concentration-dependent scavenging (56% at 40 μg/mL after 24 hours). In RSC96 cells, PG@SeQDs most effectively suppress hydrogen peroxide-induced reactive oxygen species and demonstrate time-dependent uptake with lysosomal localization and partial mitochondrial association; uptake is enhanced under inflammatory conditions (lipopolysaccharide). Collectively, PG@SeQDs represent a promising theragnostic platform for real-time reactive oxygen species imaging and management of reactive oxygen species-related inflammatory diseases, with potential for spinal cord inflammation.