MicroRNAs (miRNAs) are non‑coding RNAs (ncRNAs) that can post‑transcriptionally suppress targeted genes. Dysregulated miRNAs are associated with a variety of diseases. MiR‑181a‑5p is a conserved miRNA with the ability to regulate pathological processes, such as angiogenesis, inflammatory response and obesity. Numerous studies have demonstrated that miR‑181a‑5p exerts regulatory influence on cancer development and progression, acting as an oncomiR or tumor inhibitor in various cancer types by impacting multiple hallmarks of tumor. Generally, miR‑181a‑5p binds to target RNA sequences with partial complementarity, resulting in suppression of the targeted genes of miR‑181a‑5p. However, the precise role of miR‑181a‑5p in cancer remains incompletely understood. The present review aims to provide a comprehensive summary of recent research on miR‑181a‑5p, focusing on its involvement in different types of cancer and its potential as a diagnostic and prognostic biomarker, as well as its function in chemoresistance.

As immunosuppressive cells, Regulatory T cells (Tregs) exert their influence on tumor immune escape within the tumor microenvironment (TME) by effectively suppressing the activity of other immune cells, thereby significantly impeding the anti-tumor immune response. In recent years, the metabolic characteristics of Tregs have become a focus of research, especially the important role of lipid metabolism in maintaining the function of Tregs. Consequently, targeted interventions aimed at modulating lipid metabolism in Tregs have been recognized as an innovative and promising approach to enhance the effectiveness of tumor immunotherapy. This review presents a comprehensive overview of the pivotal role of lipid metabolism in regulating the function of Tregs, with a specific focus on targeting Tregs lipid metabolism as an innovative approach to augment anti-tumor immune responses. Furthermore, we discuss potential opportunities and challenges associated with this strategy, aiming to provide novel insights for enhancing the efficacy of cancer immunotherapy.

Background: Lung cancer is a malignant tumor with a high incidence in China, especially non-small cell lung cancer (NSCLC), which is the main threat to human life, with terrible morbidity and mortality. The research on the treatment and mechanism of NSCLC has been the forefront and hotspot of research. Recent patents show that alpha-solanine (α-solanine) exhibits the best anti-cancer activity, although its target and related mechanism remain to be elucidated. Objective: This study aims to explore the possible targets and mechanisms of α-solanine in the treatment of NSCLC through network pharmacology and experimental verification. Methods: Network pharmacology was applied to screen the possible targets of α-solanine on NSCLC, construct core networks, and perform GO enrichment and KEGG pathway analysis to predict the mechanism of α-solanine against NSCLC. Experiments were implemented to verify the results of network pharmacology in vitro. The A549 and PC-9 cells were exposed to α-solanine to assess the anti-tumor effect. Cell apoptosis was determined by the Annexin-V/PI assay. Targeted energy metabolomics was used to validate the network pharmacology results, and energy metabolism pathway- related proteins were detected by immunofluorescence and western blot. Results: Network pharmacology showed that there were 130 potential targets of α-solanine and NSCLC. GO, and KEGG analysis showed that the energy metabolism pathway is the main pathway for α-solanine to exert anti-tumor effects on NSCLC. Experimental results showed that α-solanine inhibited cell proliferation, migration, invasion and promoted cell apoptosis. At the same time, after α-solanine treatment, the energy metabolism pathway-related proteins, including GPI, ALDOA, TPI1, PKLR, LDHA, and ALDH3, were expressed reduced. In addition, α-solanine also affects the amino acid metabolism of A549 and PC-9 cells. Conclusion: Based on a combination of network pharmacological prediction and experimental verification, α-solanine may exert anti-NSCLC effects by regulating the energy metabolism pathway.

Herbal medicine has been widely applied for a range of diseases in China since antiquity. Cassia obtusifolia L. and Cassia tora L. are plants whose seeds have high reported medicinal values and have been documented to function as a laxative, to lower lipid level and to lower blood pressure. The main active ingredient in Cassia seeds is aurantio‑obtusin (AO), which is an anthraquinone monomer compound. Currently, AO is listed in China as a quality control index component of Cassia seeds. In clinical practice in China, AO is typically used to treat obesity, diabetes and its complications, non‑alcoholic fatty liver disease and allergic reactions. In addition, AO has been reported to confer insecticidal activities and antimalarial effects. Previous studies have even suggested that AO is a potential therapeutic candidate for a variety of diseases with research value. Therefore, the present review summarizes and discuss the existing literature on AO to provide a review of its pharmacological activity and mechanism of action, with the aim of providing a basis for its development and utilization in a clinical setting.

Objective: The aim of this study was to examine the effect of berberine on diabetes mellitus in vivo and in vitro, and elucidate the underlying mechanisms. Methods: Rat models of type 2 diabetes mellitus (T2DM) were established and were treated with berberine. Pathological changes in the thoracic aorta, and inflammatory factor and adiponectin levels were investigated. Vascular smooth muscle cells (VSMCs) of the thoracic aorta were cultured and treated with berberine. Cellular proliferation, migration, and inflammatory factor levels were investigated. Responses of vascular rings to phenylephrine (PE) and sodium nitroprusside (SNP) after berberine intervention and the changes of relaxation responses to SNP after adding Iberiotoxin (IbTX) were investigated. Results: Berberine ameliorated the pathological status of the thoracic aorta in the T2DM rats. Berberine significantly inhibited the C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) production, and increased the adiponectin level compared with the model group. Compared with the model group, berberine inhibited the proliferation and migration of VSMCs in vitro, and reduced tumor growth factor-β1 (TGF-β1), IL-6, and TNF-α levels. Furthermore, the contraction of thoracic aorta to PE was reduced, while the relaxation response of thoracic aorta to SNP was increased, after the berberine intervention in the T2DM rats. The relaxation response of thoracic aorta to SNP in the model and berberine groups decreased after the IbTX treatment. Conclusions: Protective effects of berberine against macrovascular complications induced by diabetes mellitus may be attributed to inhibiting of the inflammation and intervening of the calcium- activated potassium (BK_Ca).

Adoptive cell therapy (ACT) has achieved breakthrough advances in the treatment of malignancies, demonstrating particularly remarkable efficacy in hematologic cancers. However, the therapeutic efficacy of ACT remains limited by multiple factors, including low tumor antigen expression, the limited in vivo persistence of infused immune cells, and the immunosuppressive characteristics of the tumor microenvironment (TME). Meanwhile, metabolic reprogramming, a hallmark of cancer, plays a pivotal role in immune cells by directly regulating their differentiation, functional states, and long-term survival. Metabolic stress within the TME, including hypoxia, nutrient competition, and accumulation of metabolic byproducts, reshapes the metabolic states of T cells, natural killer (NK) cells, and macrophages, thereby profoundly affecting their activation, effector functions, and in vivo persistence. Consequently, a systematic understanding of how metabolic reprogramming regulates immune cell function is crucial for overcoming the current therapeutic limitations of ACT. This review systematically summarizes the metabolic constraints faced by immune effector cells in ACT and the strategies to modulate them, with a particular focus on the impact of glycolysis, lipid metabolism, amino acid homeostasis, and mitochondrial function on immune cell differentiation, effector functions, and in vivo persistence. In addition, it provides a comprehensive discussion of potential approaches to target metabolic reprogramming through pharmacological interventions and genetic engineering, aiming to overcome the metabolic limitations imposed by the TME and enhance the antitumor efficacy of ACT. While merely enhancing glycolysis can transiently increase the cytotoxic activity of immune effector cells, it often leads to metabolic exhaustion and reduced persistence. In contrast, optimizing mitochondrial function, boosting oxidative phosphorylation and fatty acid oxidation, and maintaining metabolic flexibility are more conducive to promoting memory-like phenotypes and supporting long-term survival and functional maintenance of immune cells in vivo. Future studies should integrate genetic engineering with metabolic interventions to optimize the antitumor activity of ACT in solid tumors and complex tumor microenvironments, thereby providing a theoretical foundation and translational pathway for the development of next-generation, safe and efficacious ACT therapies.