Cancer remains a formidable global public health challenge. Recent advancements in immunotherapy and targeted therapies have revolutionized diagnostic and therapeutic paradigms. Within this context, theranostics—an emerging field integrating molecular imaging with therapeutic interventions—has shown promise in achieving precision oncology. Central to theranostic platforms are dual-modality probes utilizing positron emission tomography, fluorescence, and magnetic resonance imaging technologies, which offer synergistic advantages such as complementary imaging modalities, intraoperative guidance, and real-time drug delivery monitoring. Despite growing research interest and early clinical trials, critical challenges persist in biosafety, metabolic stability, and imaging resolution. Structural optimization of probes and modality-specific selection based on cancer subtypes may address these limitations. This review systematically evaluates the design principles and clinical applications of dual-modality probes and proposes actionable strategies to enhance their translational potential.

Spinal cord injury (SCI) is a devastating condition affecting the central nervous system, often leading to persistent neurological dysfunction. While mesenchymal progenitor cells (MPCs) hold considerable promise for treating various disorders, their application in SCI repair remains hampered by challenges such as poor efficacy and safety concerns. In this study, we developed genetically engineered human MPCs with enhanced resistance to senescence and stress—termed senescence- and stress-resistant cells (SRCs)—and systematically evaluated their therapeutic potential and mechanisms in SCI repair. Intramedullary implantation of SRCs improved functional recovery after SCI. Mechanistically, SRCs exerted therapeutic effects through a dual approach: by mitigating neuronal and axonal loss while stimulating endogenous neuroregeneration, and by suppressing neuroinflammation while modulating astrocyte distribution to restrict lesion expansion. Importantly, we identified exosomes derived from SRCs as key mediators of these reparative effects. Our findings provide comprehensive insights into the therapeutic role of engineered SRCs in SCI repair, delineating both direct cellular and exosome-mediated mechanisms, thus providing experimental support for future clinical translation.

NME1 is a key metastasis suppressor whose activity depends on histidine phosphorylation, yet the biological significance of this modification remains poorly understood. Here, we reveal a previously unrecognized role for NME1 in regulating the Hippo pathway. Using PhastID-based proximity labeling combined with functional assays, we demonstrate that NME1 modulates CDC42 activity via ARHGAP17, a GTPase-activating protein, thereby influencing cytoskeletal organization and Hippo activation. Loss of NME1 reduced YAP phosphorylation and promoted its nuclear localization, indicating suppression of Hippo signaling. These findings define a histidine phosphorylation-dependent NME1–ARHGAP17–CDC42–cytoskeleton axis that controls the Hippo pathway, providing new insights into the functional repertoire of NME1 in cancer and development.

The liver, the largest glandular organ in humans, exhibits a unique and robust regenerative capacity following injury. This regenerative response is orchestrated through a highly regulated network of cellular and molecular signals. Here, we review the cytokine-mediated regulation of liver regeneration, emphasizing autocrine, paracrine, as well as endocrine pathways. Hepatocyte proliferation is modulated not only by intrinsic signals but also by cytokines derived from non-parenchymal cells—including Kupffer cells, hepatic stellate cells, and liver sinusoidal endothelial cells—as well as by endocrine cues from the systemic circulation. From the perspective of metabolic reprogramming, these regulatory pathways illustrate how adaptive changes in glucose, lipid, and amino acid metabolism collectively sustain the cellular activities essential for liver regeneration. We further explore how metabolic adaptations contribute to regeneration, providing mechanistic insights and revealing potential therapeutic targets for liver diseases. Finally, we discuss emerging strategies that target cytokine networks and metabolic pathways to enhance liver regeneration, highlighting recent advances in translational applications.