Oral cancer represents one of the most prevalent malignancies worldwide, characterized by high morbidity and mortality rates primarily due to late diagnosis, limited therapeutic efficacy, systemic toxicity, and recurrence following conventional treatments. Traditional chemotherapeutic drugs, while effective to a certain extent, often suffer from poor bioavailability, nonspecific targeting, and multidrug resistance, highlighting the importance of innovative therapeutic strategies. Nanomedicine has emerged as a promising alternative, providing site-specific delivery, enhanced drug stability, and improved therapeutic outcomes. Among various nanoparticles (NPs), metal oxide nanoparticles (MONPs), such as zinc oxide, titanium dioxide, and copper oxide, have demonstrated potent anticancer activity due to their high surface area, tunable physicochemical properties, and ability to generate reactive oxygen species (ROS). Recent progress in green synthesis approaches, employing plant extracts, microbes, and biopolymers as reducing and stabilizing agents, has further advanced the development of biocompatible and eco-friendly NPs. These green-synthesized NPs minimize toxic byproducts and allow their functionalization with herbal compounds and conventional drugs, offering synergistic effects against oral cancer. This review highlights the limitations of traditional treatments, examines the role of nanomedicine, and discusses the application of green-synthesized MONPs as drug delivery platforms for oral cancer management. It also addresses challenges such as standardization, scalability, safety concerns, and regulatory barriers, while outlining future perspectives that integrate green nanotechnology with precision medicine. Collectively, green nanomedicine offers a sustainable and innovative paradigm with the potential to revolutionize oral cancer therapy.

Female infertility and reproductive disorders represent a significant global health challenge, with complex etiologies often linked to impaired cellular communication, inflammation, and tissue dysfunction. Exosomes (EXOs), nanosized extracellular vesicles laden with bioactive molecules, have become recognized as significant transmitters of intercellular signaling in reproductive physiology and pathology. This review comprehensively discusses the dual diagnostic and therapeutic potential of EXOs in addressing female infertility disorders, such as endometriosis, polycystic ovary syndrome (PCOS), primary ovarian insufficiency (POI), Asherman syndrome, and gynecological cancers. We investigate the strategies whereby EXOs govern important activities like endometrial regeneration, folliculogenesis, immune modulation, and angiogenesis, while highlighting their role in restoring ovarian and uterine homeostasis. Advances in exosome isolation techniques, bioengineering strategies (e.g., cargo loading, surface modification), and scaffold-based delivery systems are critically evaluated for their capacity to enhance therapeutic precision and efficacy. Notwithstanding their potential, issues include standardization of isolation protocols, scalability, and long-term safety, which necessitate further research. By integrating molecular insights with translational innovations, this review underscores the clinical implementation of exosome-based therapeutics in revolutionizing reproductive medicine, offering new hope for personalized, non-invasive treatments in female fertility restoration.

Brain tumors, particularly glioblastoma, remain among the most lethal cancers, with limited survival benefits from current genetic and molecular-targeted approaches. Emerging evidence reveals that beyond oncogenes and mutations, neuronal plasticity, long-term potentiation, synaptic remodeling, and neurotransmitter-driven signaling play a pivotal role in shaping tumor progression and therapeutic response. This convergence of neuroscience and oncology has given rise to the field of cancer neuroscience, which explores the bidirectional interactions between neurons and malignant cells. In this review, we summarize fundamental principles of neuronal plasticity, contrasting physiological roles with pathological reprogramming in brain tumors. We highlight how tumor cells exploit synaptic input, particularly glutamatergic signaling, to enhance proliferation, invasion, and integration into neural circuits. We further discuss how neuronal-driven feedback loops contribute to therapy resistance, including chemoresistance, radioresistance, and immune evasion, mediated through pathways such as mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and calcium influx. The tumor microenvironment, including astrocytes, microglia, and oligodendrocyte-lineage cells, emerges as an active participant in reinforcing this neuron-tumor ecosystem. Finally, this review explores therapeutic opportunities targeting neuronal plasticity, spanning pharmacological interventions, neuromodulation approaches (transcranial magnetic stimulation (TMS), deep brain stimulation (DBS), optogenetics), and computational/artificial intelligence frameworks that model neuron tumor networks to predict personalized therapy. Also, we propose future directions integrating connect omics, neuroinformatics, and brain organoid models to refine translational strategies.

The kidney is an essential organ that has a crucial role in preserving homeostasis within the human body. Kidney cancer is considered a major clinical challenge owing to its resistance to traditional treatments such as chemotherapy, radiotherapy, and immunotherapy. Nanoparticles (NPs) gain great attention in cancer therapy due to their low toxicity, biocompatibility, and targeted drug delivery capability. This review focuses on the current role of green-synthesized NPs in renal cell carcinoma management and their applications in targeted drug delivery and cancer-specific targeting mechanisms with the demonstration of the environmentally friendly green synthesis approaches utilizing biological resources such as plant extracts and microorganisms, highlighting their advantages over conventional synthesis methods in terms of biocompatibility, sustainability, and reduced toxicity. Moreover, the therapeutic potential of nanomaterials is discussed, including magnetic NP-mediated thermal therapy, photothermal therapy, gene delivery systems, and RNA interference-based strategies. We underscore the challenges and limitations of NPs, including in vivo toxicity, biodistribution, clinical translation, large-scale production, batch-to-batch variability, long-term safety, scalability, repeatability, regulation, and reproducibility. There is growing potential to improve the treatment of kidney cancer. Hence, the promising prospects of nanotechnology in kidney cancer treatment provide a foundation for future research and clinical application. This comprehensive article highlights the significant contributions of nanomedicine to oncology and shows an optimistic perspective for more effective and precise treatment strategies for kidney cancer.

Non-alcoholic fatty pancreas (NAFP) is characterized by abnormal pancreatic fat accumulation and remains poorly understood. This study investigates the therapeutic potential and mechanistic basis of low-dose amlodipine-perindopril combination therapy, hypothesizing dual calcium channel blockade and RAS inhibition synergistically disrupt ferroptotic-inflammatory cascades driving pancreatic lipotoxicity. The bioinformatics analysis of GEO datasets (GSE40901, GSE101462, and GSE194331) identified differentially expressed genes, which were further validated through molecular docking studies with amlodipine and perindoprilat. Male Wistar rats (n = 30) were randomized into five groups: healthy control, NAFP (high-sugar/high-fat diet), amlodipine-treated, perindopril-treated, and combination therapy. Gene expression of GPX4, ACSL4, NLRP3, and rno-miR-762 was quantified by Real-Time PCR. Metabolic parameters, pancreatic histopathology, and immunohistochemical markers (caspase-1, nuclear factor kappa B (NF-κB)) were assessed. Bioinformatics analysis revealed significant alterations in ferroptosis and inflammatory pathways. Molecular docking demonstrated favorable binding affinities between therapeutic compounds and target proteins. NAFP induction resulted in GPX4 downregulation (0.471 ± 0.357 vs. 1.197 ± 0.449, P < 0.05), ACSL4 upregulation (48.633 ± 40.998 vs. 1.197 ± 0.445, p < 0.001), elevated NLRP3 (12.717 ± 7.904 vs. 1.115 ± 0.186, p < 0.001), and increased rno-miR-762 expression. The combination therapy achieved 73 % reduction in pancreatic adipocyte area (vs. 42 % with monotherapies, p < 0.001) through coordinated miR-762 suppression (↓68 %, q=0.003) and GPX4 protein restoration (↑2.1-fold, p = 0.008). NLRP3 inflammasome activity decreased by 89 % (p = 0.004). Crucially, the regimen preserved hemodynamic stability, demonstrating metabolic benefits without cardiovascular compromise. These findings position miR-762 as a linchpin biomarker connecting metabolic stress to ferroptotic pancreatitis, with clinical translation challenges. This work provides the first evidence that sub-therapeutic calcium-RAS crosstalk modulation can reverse established pancreatic steatosis while outlining a precision medicine framework for NAFP prevention.