Yang Liu

The Role of Artesunate in Cancer Management: Mechanisms of Biomedical Effects and Toxicology

Cancer remains a major global health challenge, which drives the ongoing search for effective and less toxic treatment options. Due to its demonstrated anticancer properties, Artesunate (ART), a well-established antimalarial agent, has gained increasing attention as a promising candidate for oncological applications. This systematic review provides a comprehensive evaluation of ART’s therapeutic potential by examining its anticancer efficacy, underlying molecular mechanisms, synergistic capacity, and pharmacological toxicity. An extensive search of the PubMed and Web of Science databases identified relevant peer-reviewed experimental and clinical studies that investigated ART’s anticancer activity. The data were systematically extracted with an emphasis on research methodologies, treatment regimens, and mechanistic pathways. Evidence from in vitro and in vivo studies confirms ART’s broad efficacy against a range of malignancies, including hematological cancers such as lymphoma, acute myeloid leukemia, and multiple myeloma, and various solid tumors such as lung, pancreatic, colorectal, hepatocellular, breast, ovarian, bladder, gastric, cervical, glioblastoma, melanoma, retinoblastoma, and esophageal cancers. ART exerts its anticancer effects through multiple pathways, including ROS-mediated programmed cell death, ferroptosis induction, mitochondrial dysfunction, the inhibition of proliferation, and the disruption of key signaling networks such as NF-κB, STAT3, and Wnt/β-catenin cascades. Additionally, ART has been shown to enhance the efficacy of conventional chemotherapeutic agents like cisplatin and gemcitabine while also reducing associated toxicities and overcoming drug resistance. These attributes highlight ART’s considerable potential as a versatile anticancer agent that exhibits multiple — mechanisms of action and favorable compatibility with existing therapies. However, further rigorous clinical studies are essential to fully establish its therapeutic utility and facilitate its integration into modern oncology practice.

Integrated bioinformatics analysis for the screening of hub genes and therapeutic drugs in ovarian cancer

Abstract Background Ovarian cancer (OC) ranks fifth as a cause of gynecological cancer-associated death globally. Until now, the molecular mechanisms underlying the tumorigenesis and prognosis of OC have not been fully understood. This study aims to identify hub genes and therapeutic drugs involved in OC. Methods Four gene expression profiles (GSE54388, GSE69428, GSE36668, and GSE40595) were downloaded from the Gene Expression Omnibus (GEO), and the differentially expressed genes (DEGs) in OC tissues and normal tissues with an adjusted P-value < 0.05 and a |log fold change (FC)| > 1.0 were first identified by GEO2R and FunRich software. Next, Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analyses were performed for functional enrichment analysis of these DEGs. Then, the hub genes were identified by the cytoHubba plugin and the other bioinformatics approaches including protein-protein interaction (PPI) network analysis, module analysis, survival analysis, and miRNA-hub gene network construction was also performed. Finally, the GEPIA2 and DGIdb databases were utilized to verify the expression levels of hub genes and to select the candidate drugs for OC, respectively. Results A total of 171 DEGs were identified, including 114 upregulated and 57 downregulated DEGs. The results of the GO analysis indicated that the upregulated DEGs were mainly involved in cell division, nucleus, and protein binding, whereas the biological functions showing enrichment in the downregulated DEGs were mainly negative regulation of transcription from RNA polymerase II promoter, protein complex and apicolateral plasma membrane, and glycosaminoglycan binding. As for the KEGG-pathway, the upregulated DEGs were mainly associated with metabolic pathways, biosynthesis of antibiotics, biosynthesis of amino acids, cell cycle, and HTLV-I infection. Additionally, 10 hub genes (KIF4A, CDC20, CCNB2, TOP2A, RRM2, TYMS, KIF11, BIRC5, BUB1B, and FOXM1) were identified and survival analysis of these hub genes showed that OC patients with the high-expression of CCNB2, TYMS, KIF11, KIF4A, BIRC5, BUB1B, FOXM1, and CDC20 were statistically more likely to have poorer progression free survival. Meanwhile, the expression levels of the hub genes based on GEPIA2 were in accordance with those based on GEO. Finally, DGIdb database was used to identify 62 small molecules as the potentially targeted drugs for OC treatment. Conclusions In summary, the data may produce new insights regarding OC pathogenesis and treatment. Hub genes and candidate drugs may improve individualized diagnosis and therapy for OC in future.

Molecular evidence of a clonal relationship of synchronous/multifocal gastric‐type lesions of the female genital tract

Abstract Synchronous/multifocal gastric‐type lesions (SMGLs) of the female genital tract are heterogeneous diseases that are rare and challenging to diagnose. The core issue is distinguishing between multiple primaries and multifocal metastases from a single lesion. This is vital for staging, prognosis, and treatment decisions, especially when metastases mimic primary and early lesions at the relevant sites. Traditional morphological diagnosis often faces a paradoxical situation on this key issue and cannot quantitatively evaluate the correlations among multiple foci. Here, six cases of SMGL were collected, two of which exhibited pagetoid dissemination within the genital tract, with all lesions being noninvasive. A total of 24 samples were subjected to whole‐exome sequencing. By inference based on overlapping genetic variations, base substitution mutation patterns, composition and similarity of COSMIC signatures, clonality indices, and the construction of evolutionary trees, it was inferred that the multiple foci in each patient were clonally related, indicating that all cases were metastatic. The follow‐up duration ranged from 7 to 62 months (median: 24.5 months). Four patients died of disease (median survival time: 24.5 months, range: 8–47 months), including one patient who had no invasive lesions at initial diagnosis; two patients experienced recurrences at 17 and 40 months, respectively. These results imply that even if all foci exhibit the appearance of in situ or premalignant changes histologically, they may actually be aggressive. Hence, for SMGLs, before opting for conservative treatment, comprehensive clinical assessment, appropriate surgical extent, adequate sampling, and careful microscopic examination are crucial. Clonal analysis should also be conducted where necessary to avoid undertreatment due to understaging. The study further explored the genomic traits of SMGLs involving more than two sites. © 2025 The Pathological Society of Great Britain and Ireland.

Salmonella Bacteria Membrane-Fusion Paclitaxel Loaded Liposomes for Enhanced Therapy of Intraperitoneal Metastatic Ovarian Cancer.

ABSTRACT Ovarian cancer (OvCa) remains a leading cause of gynecological cancer mortality, particularly due to its aggressive peritoneal metastasis. Conventional treatments, including surgery and paclitaxel‐based chemotherapy, are often limited by poor drug penetration into solid tumors, multidrug resistance, and the highly immunosuppressive tumor microenvironment. To overcome these challenges, we engineered a novel bacteria membrane‐fused biomimetic paclitaxel liposome (PLip@DMV) by incorporating bacteria membrane‐derived vesicles from attenuated Salmonella VNP20009. Administered via intraperitoneal injection, PLip@DMV not only delivered paclitaxel effectively but also leveraged the immunomodulatory properties of the Salmonella membrane. This led to significant antitumor immune activation within the metastatic tumor microenvironment, synergistically enhancing therapeutic efficacy and markedly prolonging the survival of tumor‐bearing mice. Furthermore, the enhanced delivery efficiency and sustained‐release characteristics of PLip@DMV resulted in significantly reduced systemic toxicity and tissue accumulation compared to free paclitaxel. Our findings demonstrate that PLip@DMV represents a more efficient, safer, and immunologically potentiated strategy for treating peritoneal metastatic ovarian cancer. This novel biomimetic nanocarrier holds significant promise for improving clinical outcomes in advanced OvCa.