Silver nanoparticles (AgNPs) play significant roles in various cancer cells such as functional heterogeneity, microenvironmental differences, and reversible changes in cell properties (e.g., chemotherapy). There is a lack of targets for processes involved in tumor cellular heterogeneity, such as metabolic clampdown, cytotoxicity, and genotoxicity, which hinders microenvironmental biology. Proteogenomics and chemical metabolomics are important tools that can be used to study proteins/genes and metabolites in cells, respectively. Chemical metabolomics have many advantages over genomics, transcriptomics, and proteomics in anticancer therapy. However, recent studies with AgNPs have revealed considerable genomic and proteomic changes, particularly in genes involved in tumor suppression, apoptosis, and oxidative stress. Metabolites interact biochemically with energy storage, neurotransmitters, and antioxidant defense systems. Mechanobiological studies of AgNPs in cancer metabolomics suggest that AgNPs may be promising tools that can be exploited to develop more robust and effective adaptive anticancer therapies. Herein, we present a proof-of-concept review for AgNPs-based proteogenomics and chemical metabolomics from various tumor cells with the help of several technologies, suggesting their promising use as drug carriers for cancer therapy.

Human vision is mediated by the retina, one of the most critical tissues in the central nervous system. Glaucoma is a complex retinal disease attributed to environmental, genetic, and stochastic factors, all of which contribute to its pathogenesis. Historically, glaucoma had been thought of primarily as a disease of the elderly; however, it is now becoming more problematic as the incidence rate increases among young individuals. In recent years, excessive light exposure has been suggested as contributing to the rise in glaucoma among the younger generation. Blue light induces mitochondrial apoptosis in retinal ganglion cells, causing optic damage; red light increases cytochrome c oxidase activity in the electron transport system, reducing inflammation and increasing antioxidant reactions to promote cell regeneration. In conclusion, the minimization of blue light exposure and the general application of red light treatment strategies are anticipated to show synergistic effects with existing treatments for retinal disease and glaucoma and should be considered a necessary prospect for the future. This review introduces the recent studies that support the relationship between light exposure and the onset of glaucoma and discusses new treatments, such as photobiomodulation therapy.

The dynamic regulation of signal transduction at plasma membrane microdomains remains poorly understood due to limitations in current experimental approaches. Genetically encoded biosensors based on fluorescent resonance energy transfer (FRET) can provide high spatiotemporal resolution for imaging cell signaling networks. Here, distinctive regulation of focal adhesion kinase (FAK) and Ca²⁺ signals are visualized at different membrane microdomains by FRET using membrane‐targeting biosensors. It is shown that rigidity‐dependent FAK and Ca²⁺ signals in human mesenchymal stem cells (hMSCs) are selectively activated at detergent‐resistant membrane (DRM or rafts) microdomains during the cell–matrix adhesion process, with minimal activities at non‐DRM domains. The rigidity‐dependent Ca²⁺ signal at the DRM microdomains is downregulated by either FAK inhibition or lipid raft disruption, suggesting that FAK and lipid raft integrity mediate the in situ Ca²⁺ activation. It is further revealed that transient receptor potential subfamily M7 (TRPM7) participates in the mobilization of Ca²⁺ signals within DRM regions. Thus, the findings provide insights into the underlying mechanisms that regulate Ca²⁺ and FAK signals in hMSCs under different mechanical microenvironments.

The RAS–RAF–MEK–ERK signaling cascade is a central component of the mitogen‐activated protein kinase (MAPK) pathway, regulating cell proliferation, differentiation, and survival, and is frequently dysregulated in cancer. Despite extensive biochemical characterization, direct observation of KRAS interactions with RAF isoforms in living cells remains limited. To overcome this limitation, a dual‐mode biosensor platform is presented that enables real‐time monitoring of RAF‐KRAS interactions through both fluorescence resonance energy transfer (FRET) and bioluminescence resonance energy transfer (BRET). Isoform‐specific biosensors reveal distinct interaction dynamics, with ARAF‐based sensors exhibiting the strongest and most reversible FRET responses. Importantly, incorporation of NanoLuc luciferase into the hybrid biosensor preserves FRET sensitivity while introducing a luminescent BRET mode suitable for high‐throughput and low‐background applications. Evaluation of oncogenic KRAS mutants indicates elevated basal FRET signals and differential binding profiles across RAF isoforms. Pharmacologic profiling further demonstrates allele‐selective inhibition, with mutant‐specific FRET and BRET responses observed upon treatment with targeted KRAS inhibitors. This biosensor platform enables live‐cell, real‐time, and quantitative monitoring of RAF‐KRAS interactions, facilitating the analysis of oncogenic signaling dynamics and the evaluation of mutation‐specific responses to targeted therapies under physiologically relevant conditions.