Aquaculture, Год журнала: 2024, Номер unknown, С. 741683 - 741683
Опубликована: Сен. 1, 2024
Язык: Английский
Aquaculture, Год журнала: 2024, Номер unknown, С. 741683 - 741683
Опубликована: Сен. 1, 2024
Язык: Английский
Genomics, Год журнала: 2025, Номер 117(2), С. 110988 - 110988
Опубликована: Янв. 5, 2025
GLP-1 receptor agonists (GLP-1RA) have been extensively utilized in the management of body weight individuals with obesity. Circular RNA (circRNA), a class covalently closed molecules, has garnered increasing attention for its potential role pathogenesis However, specific mechanisms through which circRNA contributes to GLP-1RA-induced loss remains elusive. High-throughput sequencing analyzed epididymal adipose tissue from obese mice under high-fat, and GLP-1RA intervention (600 μg/kg/d). The functions differentially expressed (DE) genes were enriched analyzed. circRNA-miRNA-mRNA interaction network was constructed Cytoscape, KEGG pathway gene enrichment validated via western blotting. A total 644 DEcircRNAs, 186 DEmiRNAs, 3474 DEmRNAs identified. Based on ceRNA score calculations, diagrams constructed. Gene Ontology (GO) analysis revealed that DERNAs linked lipid fatty acid metabolism. DE within pairs metabolism pathways, especially PI3K-Akt AMPK signaling pathways. induced phosphorylation AKT AMPK, subsequently led reduction SREBP-1, ACC, FAS. might activate pathways combat obesity circRNAs.
Язык: Английский
Процитировано
1Cellular Signalling, Год журнала: 2025, Номер 127, С. 111589 - 111589
Опубликована: Янв. 5, 2025
Язык: Английский
Процитировано
1Nature Communications, Год журнала: 2025, Номер 16(1)
Опубликована: Фев. 25, 2025
Abstract Cell death programs such as apoptosis and ferroptosis are associated with aberrant redox homeostasis linked to lipid metabolism membrane function. Evidence for cross-talk between these is emerging. Here, we show that cytotoxic stress channels polyunsaturated fatty acids via lysophospholipid acyltransferase 12 into phospholipids become susceptible peroxidation under additional stress. This reprogramming altered acyl-CoA synthetase isoenzyme expression caused by a decrease in growth factor receptor tyrosine kinase (RTK)-phosphatidylinositol-3-kinase signaling, resulting suppressed acid biosynthesis, specific stressors impaired Akt-SREBP1 activation. The reduced availability of de novo synthesized favors the channeling phospholipids. Growth withdrawal serum starvation mimics this phenotype, whereas RTK ligands counteract it. We conclude attenuated signaling during cell initiation increases cells’ susceptibility oxidative damage at interface alternative programs.
Язык: Английский
Процитировано
1Discover Oncology, Год журнала: 2024, Номер 15(1)
Опубликована: Июнь 4, 2024
Abstract Hepatocellular carcinoma (HCC), an aggressive malignancy with a dismal prognosis, poses significant public health challenge. Recent research has highlighted the crucial role of lipid metabolism in HCC development, enhanced synthesis and uptake contributing to rapid proliferation tumorigenesis cancer cells. Lipids, primarily synthesized utilized liver, play critical pathological progression various cancers, particularly HCC. Cancer cells undergo metabolic reprogramming, essential adaptation tumor microenvironment (TME), fatty acid emerging as key player this process. This review delves into intricate interplay between metabolism, focusing on four areas: de novo lipogenesis, oxidation, dysregulated immune TME, therapeutic strategies targeting for treatment.
Язык: Английский
Процитировано
5Journal of Molecular Histology, Год журнала: 2025, Номер 56(2)
Опубликована: Янв. 30, 2025
Язык: Английский
Процитировано
0Archives of Biochemistry and Biophysics, Год журнала: 2025, Номер unknown, С. 110352 - 110352
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
0Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2025, Номер unknown
Опубликована: Март 27, 2025
Язык: Английский
Процитировано
0Cancer Medicine, Год журнала: 2025, Номер 14(7)
Опубликована: Март 27, 2025
ABSTRACT Background Within the tumor microenvironment, cells undergo metabolic reprogramming of cholesterol due to intrinsic cellular alterations and changes in extracellular milieu. Furthermore, within this microenvironment influences immune landscape tumors, facilitating evasion consequently promoting tumorigenesis. These biological involve modifications numerous enzymes associated with uptake synthesis, including NPC1L1, SREBP, HMGCR, SQLE, PCSK9. Review This review systematically summarizes role metabolism its cancer progression, examines mechanisms through which dysregulation affects discusses recent advancements therapies that target metabolism. Conclusion Targeting metabolism‐related can inhibit growth, reshape landscapes, rejuvenate antitumor immunity, offering potential therapeutic avenues treatment.
Язык: Английский
Процитировано
0Cell Communication and Signaling, Год журнала: 2025, Номер 23(1)
Опубликована: Апрель 7, 2025
The cGAS-STING signaling pathway serves as a critical link between DNA sensing and innate immunity, has tremendous potential to improve anti-tumor immunity by generating type I interferons. However, STING agonists have shown decreasing biotherapeutic efficacy in clinical trials. Tumor metabolism, characterized aberrant nutrient utilization energy production, is fundamental hallmark of tumorigenesis. And modulating metabolic pathways tumor cells been discovered therapeutic strategy for tumors. As research concerning progressed, emerging evidence highlights its role reprogramming, independent immune function, indicating targets activation cancers. In this review, we delve into the interplay multiple pathways. We also synthesize current knowledge on antitumor functions STING, within microenvironment (TME) that could be exploited activation. This review necessity future dissect complex interactions with various cancer types, emphasizing personalized strategies based profiling.
Язык: Английский
Процитировано
0Aquaculture, Год журнала: 2025, Номер unknown, С. 742562 - 742562
Опубликована: Апрель 1, 2025
Язык: Английский
Процитировано
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