Wenfei Xu

Nanoparticle-driven remodeling of the Tumor Microenvironment (TME) represents a transformative strategy in cancer therapy, shifting from traditional approaches to multidimensional modulation. This review explores how engineered nanoparticles precisely target and alter key TME components—including immune cells (eg, NK cells, dendritic cells, T cells), cancer-associated fibroblasts, and the extracellular matrix—to overcome “Chemical barriers” and “physical barriers”. Furthermore, we highlight the pivotal role of nanoparticles in reprogramming TME metabolism, such as alleviating hypoxia, disrupting the Warburg effect, and modulating lipid and adenosine metabolism. By integrating immune activation with metabolic intervention, nanomedicines not only enhance anti-tumor immunity but also restore metabolic balance, offering a synergistic and potent therapeutic avenue for overcoming treatment resistance and inhibiting tumor progression.

Baicalein, a natural flavonoid derived from the root of Scutellaria baicalensis, has demonstrated antitumor efficacy in several cancers. However, its effects on human mesothelioma remain largely unclear. This study evaluates the antitumor roles and mechanisms of baicalein in mesothelioma cell lines. Effects of baicalein on mesothelioma cells phenotypic changes were investigated by measuring cell proliferation, apoptosis, migration, invasion, and cell-cycle alterations. Bioinformatic methods were applied to predict the mechanisms by which baicalien mediated its antitumor roles in mesothelioma. Crucial signaling molecules among p53-FOXM1 signaling axis, including p53, FOXM1 and cyclin B1, were evaluated by immunoblotting in mesothelioma cells. Treatment with baicalein significantly inhibited mesothelioma cell viability in a dose-dependent manner, with 48 h IC₅₀ values of 48.9 µM for MESO257 and 53.2 µM for MESO924. Baicalein also markedly reduced cell migration and invasion, while inducing apoptosis in both cell lines. Mechanistically, baicalein suppressed the p53-FOXM1 signaling axis, decreasing FOXM1 and Cyclin B1 while increasing p53 expression. Furthermore, FOXM1 overexpression attenuated the antiproliferative, anti-migratory, anti-invasive and proapoptotic effects of baicalein. Baicalein suppresses mesothelioma cell growth and invasion in vitro through modulation of the p53–FOXM1 signaling axis. These findings support its potential as a lead compound for further preclinical evaluation in mesothelioma.

Given that the sterility of urine and the urinary tract has been questioned by research, urinary microbiome dysbiosis has been recognized as one of the potential cancer-promoting factors. The composition of the urinary microbial community in healthy individuals has a relatively high similarity at the phylum level, with factors like age and gender influencing the expression and distribution. In contrast, the urinary microbiome of patients with urologic cancers shows significant variability and diversity depending on the type of cancer. Most of the early studies focused on the distribution, aggregation, and expression of microbiota in urologic cancers, warranting advanced studies on the causal relationship between microbes and urologic cancers. Bladder and prostate cancer tumorigenesis and progression can be influenced by microbes through chronic inflammatory or immunomodulatory pathways making them cancer models strongly associated with the urinary microbiome. Here, we summarize the expression characteristics of the microbiomes associated with these cancers and analyze the pathophysiological mechanisms and signaling pathways of the microbiome in the tumor promotion or suppression. By examining the role played by the urinary microbiome in the pathogenesis of urologic cancers, we assess the potential of specific microbial groups as biomarkers for diagnosis and surveillance. Additionally, involving the microbiome or using adjunctive participation in tumor therapy is becoming an emerging cancer treatment option. Improving urinary microbial homeostasis in urinary cancers by direct treatment with microbial products, microbial co-immunotherapy, probiotic-assisted therapy, and fecal microbial transplantation may broaden the scope of therapy and enhance the efficacy of conventional medicines.

This study explores the potential of ginseng-derived peptides (GPs) as multifunctional bioactive agents for skincare. Unlike previous research into ginseng saponins and polysaccharides, we identified that ginseng extracts containing water-soluble small molecules and polypeptides exhibit potent antioxidant, anti-inflammatory, and anti-aging properties. In vitro assays revealed that ginseng peptide extract (GPE) reduced reactive oxygen species (ROS) and inflammatory cytokines (IL-6, TNF-α, IL-1β) in RAW264.7 macrophages while enhancing collagen synthesis in human skin fibroblasts (HSFs). Validation using 3D epidermal and dermal models further confirmed GPE’s ability to mitigate UV-induced damage, restore skin barrier proteins (filaggrin, loricrin), and increase collagen content. In addition, we screened 19 candidate peptides from ginseng extract using machine learning and prioritized their interaction with skin aging and inflammation-related targets. Three peptides (QEGIYPNNDLYRPK, VDCPTDDATDDYRLK, and ADEVVHHPLDKSSEVE) demonstrated significant collagen-promoting, antioxidant, and anti-inflammatory effects in cellular models. These findings highlight the efficacy of computational approaches in identifying natural bioactive ingredients, positioning ginseng peptides as promising candidates for innovative cosmeceutical formulations targeting inflammaging and skin rejuvenation.