Cholesterol metabolism is crucial for cell survival and cancer progression. The prognostic patterns of genes linked to cholesterol metabolism (CMAGs) in CESC, however, have received very little attention in research. From public databases, TCGA-CESC cohorts with mRNA expression patterns and the accompanying clinical information of patients were gathered. Consensus clustering was used to find the molecular subtype connected to cholesterol metabolism. In the TCGA-CESC cohort, a predictive risk model with 28 CMAGs was created using Lasso-Cox regression. The function enrichment analysis between groups with high-and low-risk were investigated by employing GO, KEGG, and GSVA software. The immune cell infiltration was analyzed using ESTIMATE, CIBERSORT, and MCPCOUNTER methods. Finally, we select 7 genes in risk model for further multivariate Cox analysis, and ultimately a hub gene, CHIT1, was identified. Meanwhile, the function of CHIT1 was preliminarily verified in cell and mice tumor model. In conclusion, the abundance of the CHIT1 gene might be beneficial for forecasting the prognosis of CESC, demonstrating that cholesterol metabolism could be a promising treatment target for CESC.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/tox.23969 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Association between the hemoglobin A1c/High-density lipoprotein cholesterol ratio and stroke incidence: a prospective nationwide cohort study in China.
Lipids Health Dis
January 2025
Department of Neurosurgery, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213000, China.
Background: Stroke has emerged as an escalating public health challenge among middle-aged and older individuals in China, closely linked to glycolipid metabolic abnormalities. The Hemoglobin A1c/High-Density Lipoprotein Cholesterol (HbA1c/HDL-C) ratio, an integrated marker of glycolipid homeostasis, may serve as a novel predictor of stroke risk.
Methods: Our investigation utilized data from the China Health and Retirement Longitudinal Study cohort (2011-2018).
A novel variant in the ABCA1 gene for Tangier Disease with diffuse histiocytosis of bone marrow.
J Clin Lipidol
December 2024
Internal Medicine Department, Coimbra's Healthcare Integrated Delivery System, Praceta Professor Mota Pinto, 3004-561, Coimbra, Portugal.
Tangier disease is an extremely rare autosomal recessive monogenic disorder caused by mutations in the ATP binding cassette transporter A1 gene (ABCA1). It is characterized by severe deficiency or absence of high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-1 (ApoA1), with highly variable clinical presentations depending on cholesterol accumulation in macrophages across different tissues. We report a case of a 47-year-old man with very low HDL-C and very high triglyceride levels, initially attributed to the patient's metabolic syndrome, alcohol abuse, and splenomegaly.
View Article and Find Full Text PDFTimosaponin B II as a novel KEAP1-NRF2 inhibitor to alleviate alcoholic liver disease:Receptor structure-based virtual screening and biological evaluation.
Chem Biol Interact
January 2025
Anhui Prevention and Control Engineering Research Center for Fatty Liver Disease, Hefei, Anhui, 230032,P. R. China; The Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, Hefei, China; Inflammation and Immune-Mediated Diseases Laboratory of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, China. Electronic address:
Oxidative stress induced by excess ethanol is an important factor in the progression of alcoholic liver disease (ALD). In recent years, inhibiting Kelch-like ECH-associated protein 1 (KEAP1) to activate the antioxidant regulator Nuclear factor erythroid 2-related factor 2 (NRF2) has been considered an effective strategy for treating oxidative stress-related diseases, but its application in ALD remains insufficiently explored. This study aims to discover high-affinity inhibitors targeting the KEAP1 receptor.
View Article and Find Full Text PDFCellular Cholesterol Loss Impairs Synaptic Vesicle Mobility via the CAMK2/Synapsin-1 Signaling Pathway.
Front Biosci (Landmark Ed)
January 2025
Department of Neurology, Jinshan Hospital, Fudan University, 201508 Shanghai, China.
Background: Neuronal cholesterol deficiency may contribute to the synaptopathy observed in Alzheimer's disease (AD). However, the underlying mechanisms remain poorly understood. Intact synaptic vesicle (SV) mobility is crucial for normal synaptic function, whereas disrupted SV mobility can trigger the synaptopathy associated with AD.
View Article and Find Full Text PDFSERT-Deficient Mice Fed Western Diet Reveal Altered Metabolic and Pro-Inflammatory Responses of the Liver: A Link to Abnormal Behaviors.
Front Biosci (Landmark Ed)
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University of Hospital Würzburg, 97080 Würzburg, Germany.
Background: The inheritance of the short allele, encoding the serotonin transporter (SERT) in humans, increases susceptibility to neuropsychiatric and metabolic disorders, with aging and female sex further exacerbating these conditions. Both central and peripheral mechanisms of the compromised serotonin (5-HT) system play crucial roles in this context. Previous studies on SERT-deficient (Sert) mice, which model human SERT deficiency, have demonstrated emotional and metabolic disturbances, exacerbated by exposure to a high-fat Western diet (WD).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!