Chemico-Biological Interactions, Journal Year: 2024, Volume and Issue: unknown, P. 111352 - 111352
Published: Dec. 1, 2024
Language: Английский
Chemico-Biological Interactions, Journal Year: 2024, Volume and Issue: unknown, P. 111352 - 111352
Published: Dec. 1, 2024
Language: Английский
Environmental Research, Journal Year: 2025, Volume and Issue: unknown, P. 121208 - 121208
Published: Feb. 1, 2025
Language: Английский
Citations
1Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)
Published: Jan. 10, 2025
Abstract Cadmium has been identified as an environmental pollutant and a carcinogen. N 6 -methyladenosine (m A) plays crucial role in the development of lung tumors, but mechanisms remain incompletely clarified. In present study, our data demonstrated that prolonged treatment 1 μmol/L CdSO 4 for 40 passages bronchial epithelial cells (Beas-2B cells) resulted malignant phenotype, which manifested boosted proliferation, migration invasion capacity well apoptosis reduction. Proteomic assay revealed passage cells, 350 proteins showed differentially expressed comparison to control, these were primarily enriched Kyoto Encyclopedia Genes Genomes (KEGG) pathways “pathways cancer” “Chemical carcinoma-reactive oxygen species”. Moreover, mRNAs Nuclear factor kappa B ( NF-κB) p65 NAD(P)H: quinone oxidoreductase (NQO1) , key signaling molecules two pathways, predicted contain m A modification sites with high confidence. The subsequent experimental results indicated levels Fat mass obesity associated protein (FTO) elevated, while Alkylated DNA repair alkB homolog 5 (ALKBH5) YTH Domain Containing Protein 2 (YTHDC2) reduced increasing cadmium generations. Furthermore, reduction by 3-deazide adenosine (DAA, inhibitor) was found significantly inhibit characteristics cadmium-induced activate involved nuclear erythroid 2-related (NRF2) pathway, activity NF-κB. It is also noteworthy based on animals indicate relevant indicators biological changes are partially similar cell experiments. detail, tissue observed increase expressions FTO, ALKBH5 YTHDC2 drop. Additionally, immunofluorescence examination illustrated co-localization regulatory FTO presented collectively suggest chronic may impact level through influencing proteins, could potentially trigger oxidative stress regulating transcription factors such NF-κB NRF2. conclusion, study provides scientific foundation understanding toxicity offers novel insights treating diseases.
Language: Английский
Citations
0BMC Cancer, Journal Year: 2025, Volume and Issue: 25(1)
Published: March 24, 2025
This study aimed to elucidate the expression profile and biological implications of peroxidase 5 (PRDX5) in bladder cancer (BC), specifically investigating its influence on BC progression through modulation reactive oxygen species (ROS) levels activation ferroptosis pathways. We employed urine proteomics data transcriptomic information from Cancer Genome Atlas (TCGA) identify differentially expressed genes tissues, focusing PRDX5. Using single-cell RNA sequencing (scRNA-seq), we assessed PRDX5 distribution across various cell types tumor microenvironment. conducted vitro experiments analyze impact proliferation, migration, invasion, while exploring mechanisms modulating ROS ferroptosis. In vivo were performed observe PRDX5's signaling tissue contexts. found significant upregulation with scRNA-seq revealing enrichment epithelial cells, correlating disease advancement established markers. analyses showed that overexpressed enhanced invasion knockout produced opposing effects. Additionally, modulated impacted confirmed inhibited growth activated pathways tissues. Our highlights elevated role promoting regulation may serve as a promising target for treatment, supporting further exploration potential clinical applications.
Language: Английский
Citations
0Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 469, P. 133983 - 133983
Published: March 8, 2024
Language: Английский
Citations
1Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 480, P. 136243 - 136243
Published: Oct. 23, 2024
Language: Английский
Citations
1Environment International, Journal Year: 2024, Volume and Issue: 190, P. 108819 - 108819
Published: June 14, 2024
Emerging evidence has linked arsenic exposure and metabolic homeostasis, but the mechanism is incompletely understood, especially at relatively low concentrations. In this study, we used a mouse model to evaluate health impacts toxicity of in drinking water environmentally relevant levels (0.25 1.0 ppm). Our results indicated that damaged intestinal barrier induced accumulation, oxidative stress, pathological changes liver illum. Interestingly, increased hepatic triglyceride (TG) total cholesterol (TC), while reduced serum TG TC levels. The transcriptome found caused perturbation promoted lipid accumulation by regulating exogenous fatty acids degradation apolipoproteins related genes. metabolomics identified 74 88 differential metabolites 0.25 ppm, respectively. KEGG disease subcellular location analysis diseases, mitochondrion might be target organelle for arsenic-induced toxicity. Co-enrichment metabolome 24 9 genes as biomarkers. Moreover, 40 male (20 nonalcoholic (NAFLD) cases 20 healthy controls) was further selected validate our findings. Importantly, significantly changed L-palmitoylcarnitine, 3-hydroxybutyric acid, 2-hydroxycaproic acid 6 Hadha, Acadl, Aldh3a2, Cpt1a, Cpt2, Acox1 were NAFLD cases. from integrated multi-omics chemical-protein network L-palmitoylcarnitine played critical role mitochondrial β-oxidation (Cpt1a, Cpt2). conclusion, these findings provided new clues levels, which involved late-life development. also contribute understanding human responses phenotypic hazardous material environment.
Language: Английский
Citations
0International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(17), P. 9316 - 9316
Published: Aug. 28, 2024
Newborn lambs are susceptible to pathogenic bacterial infections leading enteritis, which affects their growth and development causes losses in sheep production. It has been reported that N6-methyladenosine (m6A) is closely related innate immunity, but the effect of m6A on small intestinal epithelial cells (IECs) mechanism involved have not elucidated. Here, we investigated effects lipopolysaccharide (LPS)-induced inflammatory responses, apoptosis oxidative stress primary IECs. First, extracted IECs were identified by immunofluorescence using cell signature protein cytokeratin 18 (
Language: Английский
Citations
0Environmental Research, Journal Year: 2024, Volume and Issue: 263, P. 120139 - 120139
Published: Oct. 10, 2024
Language: Английский
Citations
0Chemico-Biological Interactions, Journal Year: 2024, Volume and Issue: unknown, P. 111352 - 111352
Published: Dec. 1, 2024
Language: Английский
Citations
0