PubMed HealthSearch

Biomedical subjects

Dawei Wang

Publications and source records attributed to Dawei Wang.

3 recordsLinked to original sources

Unveiling phthalate esters biodegradation from microbial community to Pseudarthrobacter scleromae HL-1: Kinetics, genomic insights, pathways, toxicity assessment and environmental remediation.

Phthalate esters (PAEs) are ubiquitous synthetic plasticizer pollutants posing severe ecological and human health risks. This study compared microbial community structures and dibutyl phthalate (DBP) degradation kinetics of two consortia: 7-day enriched MC1 (50 mg/L DBP) and 6-cycle acclimated MC7 (50-1000 mg/L DBP), demonstrating directional DBP stress selection generated a low-diversity, highly specialized degradative community with a 25.4 mg/L/h maximum degradation rate (Vmax), 1.68-fold higher than MC1. Four dominant DBP-degrading strains were isolated from MC7; Pseudarthrobacter scleromae HL-1 showed the highest efficiency with 17.1 mg/L/h Vmax and complete 500 mg/L DBP removal within 72 h, broad substrate spectrum, and strong adaptability after optimization. Whole-genome sequencing and GC-MS/MS elucidated a dual-parallel DBP mineralization pathway, first reported in Pseudarthrobacter, integrating ester hydrolysis and side-chain β-oxidation. ECOSAR and Chlorella vulgaris bioassays confirmed progressive toxicity attenuation, with > 99% relative toxicity reduction after 72 h and no toxic intermediate accumulation. Natural lake water trials with trace background PAEs showed HL-1 successfully colonized aquatic environments, reshaped indigenous communities into synergistic degradative consortia, and achieved 99.2% DBP removal in 84 h. This work provides comprehensive insights into PAE biodegradation mechanisms from community to single strain and highlights HL-1 as a promising candidate for remediating PAE-polluted aquatic ecosystems.

Genomic analysis

Syncytium-forming HSV-1 in cancer gene therapy: From molecular mechanisms to clinical translation.

Gene therapy has emerged as a promising strategy for cancer treatment, yet challenges in efficient gene delivery remain a major barrier. Herpes simplex virus type 1 (HSV-1), as an oncolytic virus, has garnered attention for its potential in cancer therapy due to its replicative capacity, large genomic payload, and relatively low toxicity. Notably, syncytium-forming HSV-1 (SF-HSV-1) not only exhibits enhanced and sustained antitumor efficacy but also triggers profound immune responses. However, the exact molecular mechanisms orchestrating HSV-1-induced syncytium formation, its resulting cytotoxicity, and its precise role in immune modulation remain incompletely understood. This review aims to provide an in-depth exploration of the mechanisms underlying HSV-1 syncytium formation and its therapeutic implications in cancer gene therapy.

Humans

PPRC1 is a prognostic biomarker and key regulator of mitochondrial oxidative phosphorylation in multiple myeloma.

BACKGROUND: Multiple myeloma (MM) remains an incurable haematological malignancy, underscoring the need for novel prognostic biomarkers and therapeutic targets. This study aimed to investigate the clinical and biological significance of peroxisome proliferator-activated receptor gamma coactivator-related protein 1 (PPRC1) in MM. METHODS: Expression and clinical data were obtained from public databases and an independent local cohort. Kaplan-Meier and Cox regression analyses were performed to evaluate prognostic value. Differential expression analysis, pathway enrichment analysis and single-cell RNA-seq data analysis were used to explore biological functions. PPRC1 was silenced in MM cell lines using siRNA to assess its effects on cell survival and oxidative phosphorylation. RESULTS: PPRC1 was significantly upregulated in MM and was associated with advanced disease stage and poor overall survival. Multivariate Cox analysis identified PPRC1 as an independent prognostic factor. A nomogram incorporating PPRC1 and revised-ISS improved survival prediction. Functional analyses revealed that PPRC1 was positively correlated with oxidative phosphorylation and oncogenic signalling pathways. A potential connection between PPRC1 expression and immune cell infiltration was observed. PPRC1 knockdown inhibited cell proliferation, induced cell cycle arrest and apoptosis and impaired oxidative phosphorylation in MM. CONCLUSIONS: PPRC1 acts as a prognostic biomarker and metabolic regulator in MM by sustaining mitochondrial oxidative phosphorylation. These findings highlight PPRC1 as a potential therapeutic target in MM.

Humans