The online version contains supplementary material available at 10.1007/s10616-026-00968-y.

The fat mass and obesity-associated protein (FTO), an N6-methyladenosine (m6A) demethylase, plays a crucial role in various cancers. This study investigates its expression and functional role in bladder cancer (BCa). Analysis of TCGA data and validation in BCa cell lines revealed that FTO is significantly overexpressed in bladder cancer tissues and is associated with poor overall and disease-free survival. Functional assays demonstrated that knockdown of FTO markedly increased global m6A RNA methylation and suppressed the proliferation, migration, invasion, and colony formation of BCa cells in vitro. Furthermore, FTO depletion significantly inhibited tumor growth and experimental liver colonization in nude mouse xenograft models. Mechanistically, transcriptomic analysis of FTO-high patient tissues and FTO-knockdown cells revealed a strong association between FTO and epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) pathways. Consequently, FTO knockdown impaired the self-renewal capacity of BCa cells and downregulated the expression of key stemness genes (CD133, CD44, Nanog, OCT4). These findings suggest FTO is a critical oncoprotein that promotes bladder cancer progression and stemness-associated phenotypes, highlighting its potential as a therapeutic target and prognostic marker.

Infections, injuries, or surgeries that remove bone can cause bone abnormalities that require specific biomaterials to promote blood vessel growth and bone healing. Composite nanoparticles made of strontium-doped beta-tricalcium phosphate (Sr-doped ß-TCP) are a versatile nanomaterial that could be used in healthcare, especially for repairing bone tissue and tackling antimicrobial resistance (AMR). Strontium, a metal, is known to enhance osteogenesis and fight pathogenic agents. It may also influence bacterial metabolic processes, helping to reduce antibiotic resistance. We produced Sr-doped ß-TCP and its composites using Continuous Plastic Flow Synthesis (CPFS) and autoclaving. Electrospinning created nanofiber composites. FTIR spectroscopy, particle size analysis, zeta potential measurement, XRD, and SEM studies characterized these materials. Their antibacterial activity was tested against Escherichia coli and Staphylococcus aureus with the agar well diffusion assay. For vivo tests, a 3mm defect was made in the right tibia of rabbits and then treated with the Sr-doped ß-TCP composite. The rabbits were observed at 2, 4, and 6 weeks after surgery. Histological analysis involved decalcifying the specimens, and imaging was performed with an electron microscope. A toxicity assessment of Sr-doped ß-TCP was conducted on BHK-21 fibroblastic cells.

The online version contains supplementary material available at 10.1007/s10616-026-00985-x.

This study explores the biological and pharmacological potential of Inula aschersoniana Janka (I. aschersoniana) by utilizing both in silico computational and in vitro analyses, focusing on anticancer, antioxidant, and enzyme inhibitory activities. I. aschersoniana extracts were observed to have effective properties against breast cancer (MCF-7) and human colon adenocarcinoma (HT-29) cell lines compared to normal human umbilical vein endothelial (HUVEC) cell line. Also, effective antioxidant activity of the plant sample was determined by using several in vitro antioxidant methods. Furthermore, inhibitory effects of I. aschersoniana extracts against alpha-glucosidase (α-Gly) and glutathione S-transferase (GST) enzymes were evaluated. The IC50 value of I. aschersoniana ethyl acetate extract was determined as 4.05µg/mL for α-Gly and 1.67µg/mL for GST. Similarly, IC₅₀ value of the ethanol extract was measured as 3.74µg/mL for α-Gly and 2.71µg/mL for GST. Also, main organic compounds of I. aschersoniana were detected to be vanillic acid, rutin, and naringin by HPLC technique. Finally, integrated network pharmacology, molecular docking, and molecular dynamics simulations were performed to elucidate the potential interactions between the active components of I. aschersoniana and genes associated with breast and colon cancer. To ensure reliability, molecular docking results were validated using re-docking and comparison with reference inhibitors or co-crystallized ligands. RMSD and RMSF analyses revealed that naringin, the major compound of I. aschersoniana, exhibited dynamically stable binding within the active sites of AKT1, EGFR, and PPARG proteins, with AKT1@Naringin and PPARG@Naringin complexes displaying a more stable dynamic profile. In this network pharmacology study, forty-five common targets between the major compounds of I. aschersoniana with breast and colon cancers were identified.

Viscum coloratum (Kom.) Nakai has been widely used in traditional Chinese medicine and clinical treatment mainly for rheumatoid arthritis (RA). Our latest study demonstrated that it could alleviate clinical symptoms of RA and decrease osteoclastogenesis-related gene expression in the CIA mouse model. However, whether Viscum coloratum (Kom.) Nakai could inhibit osteoclastogenesis and its underlying mechanisms need to be further elucidated. In this study, we demonstrated that extract of Viscum coloratum (Kom.) Nakai (EVC) exhibited extraordinary activity against RANKL-induced osteoclast differentiation identified by inhibiting the formation of TRAP-positive multinucleated osteoclasts, TRAP activity, and decreasing osteoclast-specific genes NFATc1 expression. The network pharmacology-based method integrating Protein-Protein interaction analysis revealed that Viscum coloratum (Kom.) Nakai could inhibit osteoclastogenesis by regulating PI3K-AKT signaling pathways. Then, the predicted signaling pathway of EVC on osteoclast differentiation was determined by Western blot. Using TRAP activity and nitric oxide assays, Viscumneoside III, which was identified as the main ingredient from Viscum coloratum (Kom.) Nakai in our previous study, was confirmed as the primary effective ingredient. These findings reveal that EVC executed the traditional effects on strengthening muscles and bones for the treatment of RA by inhibiting osteoclastogenesis via the regulated PI3K/AKT/mTOR signaling pathway, and Viscumneoside III was its effective ingredient.

Pesticides are among the most effective tools for pest control; however, their use involves significant exposure to toxic agents, and their use implies significant risks to human health and the environment. The present scientometric analysis and systematic review highlight the genotoxic and cytotoxic effects of pesticides with Organophosphates and Neonicotinoids being among the most relevant classes studied, which are linked mainly to mechanisms such as oxidative stress and DNA damage in human, animal and plant cells. Through biomarkers and standardized techniques such as comet and micronucleus assays, the correlation of these compounds in the generation of mutations and genetic alterations has been confirmed, with critical implications for public and environmental health. Additional research has evolved toward more precise approaches conducted by international collaboration and a special interest in emerging countries. This study highlights the need for stricter regulation, the development of less toxic pesticides considering other alternatives such as biopesticides, strategies to mitigate associated risks, and the establishment of a solid foundation for future research and sustainable policies.

To investigate the effect of Ursolic acid (UA) on liver cancer cells through cell experiments, in order to inhibit cell proliferation and induce apoptosis. By adding z-vad-fmk apoptosis inhibitor and ROS inhibitor NAC, CCK8, cell apoptosis, Western blot experiments, mitochondrial membrane potential detection, and ROS flow cytometry were conducted. Compared with the positive drug sorafenib, the inhibitory effect of UA on liver cancer cells and its promotion of apoptosis were studied. The results of CCK8 confirmed that when UA was at its optimal concentration, its inhibitory effect on liver cancer cell viability was greater than that of sorafenib; Through cell apoptosis experiments, it can be observed that under fluorescence microscopy, the fluorescence intensity in the UA+HepG2 group is significantly stronger than that in the sorafenib+HepG2 group; Western blot experiments showed that the relative expression levels of proteins in HepG2 were almost equal between the HepG2+UA and sorafenib+HepG2 groups; through ROS experiments, it was found that when the reactive oxygen species in the HepG2+UA group were lower than those in the sorafenib+HepG2 group, it indicated that the former had a stronger effect of UA on HepG2. UA has a significant inhibitory effect on proliferation and promotes apoptosis in liver cancer cells.

The online version contains supplementary material available at 10.1007/s10616-026-00912-0.