Hong Li

NCAPH is upregulated in endometrial cancer and associated with poor clinicopathologic characteristics

AbstractBackgroundRecently, NCAPH (non‐SMC condensin I complex subunit H), a regulatory subunit of the condensin complex, has captured our attention in various cancer studies. However, the function of NCAPH in endometrial cancer (EC) remains unclear. Our study aims to investigate the role of NCAPH in EC.MethodsThe expression of NCAPH in EC tissues and normal tissues was predicted by The Cancer Genome Atlas (TCGA). The Kaplan–Meier analysis was performed to evaluate the impact of NCAPH expression on EC patients’ survival. Logistic regression was used to study the correlation of NCAPH expression with clinicopathologic characteristics. Molecular mechanisms behind NCAPH in EC were evaluated by Gene Set Enrichment Analysis, genetic mutations, copy number variation, and DNA methylation level.ResultsNCAPH was significantly upregulated in EC (p = 1e−24), and its expression level was significantly related to the more advanced International Federation of Gynecology & Obstetrics (FIGO) stage (stage IV vs. stage I: odd ratio.[OR] = 3.7), higher grade (poor vs. well & moderate: OR = 5.3), serous histology subtype (SEA vs. EEA: OR = 8.5), myometrial invasion (≥50 vs. < 50 invasion: OR = 1.8), metastasis (vs. no metastasis: OR = 2.5), and with‐tumor status (vs. free of tumor: OR = 2.3) (all p were less than .05). The Gene Set Enrichment Analysis method indicated that MITOTIC_SPINDLE, G2M_CHECKPOINT, MYC_TARGETS_V1, E2F_TARGETS, MYC_TARGETS_V2, and MTORC1_SIGNALING were involved in the upregulated NCAPH group. NCAPH hypomethylation, amplified copy number variations and genetic mutations; all played a contributive role in NCAPH upregulation.ConclusionsThese results reveal NCAPH functions as oncogene and promote the development of EC.

Engineering Magnetic Extracellular Vesicles Mimetics for Enhanced Targeting Chemodynamic Therapy to Overcome Ovary Cancer

Chemodynamic therapy (CDT), employing metal ions to transform endogenous H

Engineering Extracellular Vesicles Mimetics for Targeted Chemotherapy of Drug-Resistant Ovary Cancer

Oxygen-Generating Hydrogels Overcome Tumor Hypoxia to Enhance Photodynamic/Gas Synergistic Therapy

Hypoxic environment is a bottleneck of photodynamic therapy (PDT) in tumor treatment, as oxygen is the critical substrate for photosensitivity reaction. Herein, a sustained oxygen supply system based on cerium nanoparticles and hydrogel (GHCAC) was explored for enhanced synergistic PDT and gas therapy. Ceria nanoparticles were prepared as a drug carrier by self-assembly mediated by hyaluronic acid (HA), a targeting for CD44 on cervical cancer cells, followed by photosensitizer and l-arginine (l-Arg) loading. Then, the GHCAC system was developed by incorporating a prepared nanocarrier (HCePA) and O

The Role of Gut Microbiota and Their Derived Metabolites in Chemotherapy‐Induced Nausea and Vomiting in Ovarian Cancer

ABSTRACT Objective This study aimed to investigate the relationship between gut microbiota and chemotherapy‐induced nausea and vomiting (CINV) in patients with ovarian cancer undergoing platinum‐based chemotherapy (carboplatin or cisplatin combined with paclitaxel). Methods Clinical data and fecal samples were collected from patients with ovarian cancer after admission but prior to the initiation of their first chemotherapy cycle. Patients were divided into the CINV ( n  = 25) and non‐CINV ( n  = 25) groups on the basis of symptoms occurring after chemotherapy. No additional samples were collected during chemotherapy. Integrated metagenomic sequencing and untargeted metabolomic profiling identified CINV‐associated microbial taxa and metabolites. Additionally, fecal microbiota transplantation (FMT) in SD rats validated causal links between gut dysbiosis and CINV pathogenesis. Results Bacteroides caccae , Corynebacteriales, and Corynebacterium were significantly enriched in the CINV group. KEGG enrichment revealed upregulated pathways in CINV, including focal adhesion, lysosome function, and eukaryotic cellular communities. Metabolomic analysis identified 19 significantly increased metabolites in the fecal samples of CINV patients versus 10 in non‐CINV controls. KEGG enrichment revealed that the pentose phosphate pathway, glutathione metabolism, and lipoic acid metabolism were significantly implicated in CINV pathogenesis. Multi‐omics integration revealed Bacteroides sp. A1C1 strongly correlated with hesperetin, arbutin, orciprenaline, and myristolic acid. In rats, cisplatin‐induced CINV models showed higher kaolin consumption versus controls ( p  < 0.05). FMT from non‐CINV donors reduced kaolin consumption in cisplatin‐treated rats ( p  < 0.05). The expression of 5‐HT3R, NK1R, and NK2R in the medulla oblongata and colon was significantly increased in the cisplatin model group ( p  < 0.05) and partially reversed by non‐CINV FMT ( p  < 0.05). Conclusions Gut microbiota dysbiosis directly contributes to CINV pathogenesis. Bacteroides sp. A1C1 and its putatively identified metabolites (hesperetin, arbutin, orciprenaline, and myristolic acid) represent potential diagnostic biomarkers for CINV.