1. A novel LGALS1-depended and immune-associated fatty acid metabolism risk model in acute myeloid leukemia stem cells.
- Author
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Qin H, Peng M, Cheng J, Wang Z, Cui Y, Huang Y, Gui Y, Sun Y, Xiang W, Huang X, Huang T, Wang L, Chen J, and Hou Y
- Subjects
- Humans, Male, Animals, Female, Mice, Risk Factors, Tumor Microenvironment, Cell Line, Tumor, Apoptosis, Cell Proliferation, Prognosis, Middle Aged, Leukemia, Myeloid, Acute metabolism, Leukemia, Myeloid, Acute pathology, Leukemia, Myeloid, Acute genetics, Galectin 1 metabolism, Galectin 1 genetics, Fatty Acids metabolism, Neoplastic Stem Cells metabolism, Neoplastic Stem Cells pathology
- Abstract
Leukemia stem cells (LSCs) are recognized as the root cause of leukemia initiation, relapse, and drug resistance. Lipid species are highly abundant and essential component of human cells, which often changed in tumor microenvironment. LSCs remodel lipid metabolism to sustain the stemness. However, there is no useful lipid related biomarker has been approved for clinical practice in AML prediction and treatment. Here, we constructed and verified fatty acid metabolism-related risk score (LFMRS) model based on TCGA database via a series of bioinformatics analysis, univariate COX regression analysis, and multivariate COX regression analysis, and found that the LFMRS model could be an independent risk factor and predict the survival time of AML patients combined with age. Moreover, we revealed that Galectin-1 (LGALS1, the key gene of LFMRS) was highly expressed in LSCs and associated with poor prognosis of AML patients, and LGALS1 repression inhibited AML cell and LSC proliferation, enhanced cell apoptosis, and decreased lipid accumulation in vitro. LGALS1 repression curbed AML progression, lipid accumulation, and CD8
+ T and NK cell counts in vivo. Our study sheds light on the roles of LFMRS (especially LGALS1) model in AML, and provides information that may help clinicians improve patient prognosis and develop personalized treatment regimens for AML., (© 2024. The Author(s).)- Published
- 2024
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