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1.
Sci Rep ; 14(1): 15758, 2024 07 09.
Article in English | MEDLINE | ID: mdl-38977800

ABSTRACT

The role of SLC3A2, a gene implicated in disulfidptosis, has not been characterized in gliomas. This study aims to clarify the prognostic value of SLC3A2 and its influence on glioma. We evaluated the expression of SLC3A2 and its prognostic importance in gliomas using publicly accessible databases and our clinical glioma samples and with reliance on Meta and Cox regression analysis approaches. Functional enrichment analyses were performed to explore SLC3A2's function. Immune infiltration was evaluated using CIBERSORT, ssGSEA, and single-cell sequencing data. Additionally, Tumor immune dysfunction and exclusion (TIDE) and epithelial-mesenchymal transition scores were determined. CCK8, colony formation, migration, and invasion assays were utilized in vitro, and an orthotopic glioma xenograft model was employed in vivo, to investigate the role of SLC3A2 in gliomas. Bioinformatics analyses indicated high SLC3A2 expression correlates with adverse clinicopathological features and poor patient prognosis. Upregulated SLC3A2 influenced the tumor microenvironment by altering immune cell infiltration, particularly of macrophages, and tumor migration and invasion. SLC3A2 expression positively correlated with immune therapy indicators, including immune checkpoints and TIDE. Elevated SLC3A2 was revealed as an independent risk element for poor glioma prognosis through Cox regression analyses. In vitro experiments showed that reduced SLC3A2 expression decreased cell proliferation, migration, and invasion. In vivo, knockdown of SLC3A2 led to a reduction in tumor volume and prolonged survival in tumor-bearing mice. Therefore, SLC3A2 is a prognostic biomarker and associated with immune infiltration in gliomas.


Subject(s)
Brain Neoplasms , Gene Expression Regulation, Neoplastic , Glioma , Glioma/genetics , Glioma/pathology , Glioma/metabolism , Humans , Prognosis , Animals , Mice , Cell Line, Tumor , Brain Neoplasms/genetics , Brain Neoplasms/pathology , Brain Neoplasms/metabolism , Brain Neoplasms/immunology , Cell Movement , Tumor Microenvironment/immunology , Cell Proliferation , Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Fusion Regulatory Protein 1, Heavy Chain/genetics , Fusion Regulatory Protein 1, Heavy Chain/metabolism , Female , Male , Epithelial-Mesenchymal Transition/genetics , Mice, Nude
2.
Environ Pollut ; 343: 123215, 2024 Feb 15.
Article in English | MEDLINE | ID: mdl-38145635

ABSTRACT

The cooking fumes generated from thermal cooking oils contains various of hazardous components and shows deleterious health effects. The edible oil refining is designed to improve the oil quality and safety. While, there remains unknown about the connections between the characteristics and health risks of the cooking fumes and oils with different refining levels. In this study, the hazardous compounds, including aldehydes, ketones, polycyclic aromatic hydrocarbons (PAHs), and particulate matter (PM) in the fumes emitted from heated soybean oils with different refining levels were characterized, and their health risks were assessed. Results demonstrated that the concentration range of aldehydes and ketones (from 328.06 ± 24.64 to 796.52 ± 29.67 µg/m3), PAHs (from 4.39 ± 0.19 to 7.86 ± 0.51 µg/m3), and PM (from 0.36 ± 0.14 to 5.08 ± 0.15 mg/m3) varied among soybean oil with different refining levels, respectively. The neutralized oil showed the highest concentration of aldehydes and ketones, whereas the refined oil showed the lowest. The highest concentration levels of PAHs and PM were observed in fumes emitted from crude oil. A highly significant (p < 0.001) positive correlation between the acid value of cooking oil and the concentrations of PM was found, suggesting that removing free fatty acids is critical for mitigating PM concentration in cooking fumes. Additionally, the incremental lifetime cancer risk (ILCR) values of PAHs and aldehydes were 5.60 × 10-4 to 8.66 × 10-5 and 5.60 × 10-4 to 8.66 × 10-5, respectively, which were substantially higher than the acceptable levels (1.0 × 10-6) established by US EPA. The present study quantifies the impact of edible oil refining on hazardous compound emissions and provides a theoretical basis for controlling the health risks of cooking fumes via precise edible oil processing.


Subject(s)
Polycyclic Aromatic Hydrocarbons , Soybean Oil , Soybean Oil/analysis , Plant Oils , Polycyclic Aromatic Hydrocarbons/analysis , Particulate Matter , Gases/analysis , Risk Assessment , Cooking/methods , Aldehydes/analysis , Ketones/analysis
3.
Cell Regen ; 10(1): 15, 2021 Mar 19.
Article in English | MEDLINE | ID: mdl-33740162

ABSTRACT

BACKGROUND: The pluripotent stem cells in planarians, a model for tissue and cellular regeneration, remain further identification. We recently developed a method to enrich piwi-1+ cells in Schmidtea mediterranea, by staining cells with SiR-DNA and Cell Tracker Green, named SirNeoblasts that permits their propagation and subsequent functional study in vivo. Since traditional enrichment for planarian neoblasts by Hoechst 33342 staining generates X1 cells, blocking the cell cycle and inducing cytotoxicity, this method by SiR-DNA and Cell Tracker Green represents a complementary technological advance for functional investigation of cell fate and regeneration. However, the similarities in heterogeneity of cell subtypes between SirNeoblasts and X1 remain unknown. RESULTS: In this work, we performed single cell RNA sequencing of SirNeoblasts for comparison with differential expression patterns in a publicly available X1 single cell RNA sequencing data. We found first that all of the lineage-specific progenitor cells in X1 were present in comparable proportions in SirNeoblasts. In addition, SirNeoblasts contain an early muscle progenitor that is unreported in X1. Analysis of new markers for putative pluripotent stem cells identified here, with subsequent sub-clustering analysis, revealed earlier lineages of epidermal, muscular, intestinal, and pharyngeal progenitors than have been observed in X1. Using the gcm as a marker, we also identified a cell subpopulation resided in previously identified tgs-1+ neoblasts. Knockdown of gcm impaired the neoblast repopulation, suggesting a function of gcm in neoblasts. CONCLUSIONS: In summary, the use of SirNeoblasts will enable broad experimental advances in regeneration and cell fate specification, given the possibility for propagation and transplantation of recombinant and mutagenized pluripotent stem cells that are not previously afforded to this rapid and versatile model system.

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