Chemico-Biological Interactions, Год журнала: 2024, Номер unknown, С. 111352 - 111352
Опубликована: Дек. 1, 2024
Язык: Английский
Chemico-Biological Interactions, Год журнала: 2024, Номер unknown, С. 111352 - 111352
Опубликована: Дек. 1, 2024
Язык: Английский
Environmental Research, Год журнала: 2025, Номер unknown, С. 121208 - 121208
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
1Cell Death Discovery, Год журнала: 2025, Номер 11(1)
Опубликована: Янв. 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.
Язык: Английский
Процитировано
0BMC Cancer, Год журнала: 2025, Номер 25(1)
Опубликована: Март 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.
Язык: Английский
Процитировано
0Journal of Hazardous Materials, Год журнала: 2024, Номер 469, С. 133983 - 133983
Опубликована: Март 8, 2024
Язык: Английский
Процитировано
1Journal of Hazardous Materials, Год журнала: 2024, Номер 480, С. 136243 - 136243
Опубликована: Окт. 23, 2024
Язык: Английский
Процитировано
1Environment International, Год журнала: 2024, Номер 190, С. 108819 - 108819
Опубликована: Июнь 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.
Язык: Английский
Процитировано
0International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(17), С. 9316 - 9316
Опубликована: Авг. 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 (
Язык: Английский
Процитировано
0Environmental Research, Год журнала: 2024, Номер 263, С. 120139 - 120139
Опубликована: Окт. 10, 2024
Язык: Английский
Процитировано
0Chemico-Biological Interactions, Год журнала: 2024, Номер unknown, С. 111352 - 111352
Опубликована: Дек. 1, 2024
Язык: Английский
Процитировано
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