A lipid metabolism-related genes prognosis biomarker associated with the tumor immune microenvironment in colorectal carcinoma

Lipid metabolic reprogramming is considered to be a new hallmark of malignant tumors. The purpose of this study was to explore the expression profiles of lipid metabolism-related genes (LMRG) in colorectal cancer (CRC). The lipid metabolism statuses of 500 CRC patients from the Cancer Genome Atlas (...

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Veröffentlicht in:BMC cancer 2021-11, Vol.21 (1), p.1182-1182, Article 1182
Hauptverfasser: Yang, Chao, Huang, Shuoyang, Cao, Fengyu, Zheng, Yongbin
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Sprache:eng
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Zusammenfassung:Lipid metabolic reprogramming is considered to be a new hallmark of malignant tumors. The purpose of this study was to explore the expression profiles of lipid metabolism-related genes (LMRG) in colorectal cancer (CRC). The lipid metabolism statuses of 500 CRC patients from the Cancer Genome Atlas (TCGA) and 523 from the Gene Expression Omnibus (GEO GSE39582) database were analyzed. The risk signature was constructed by univariate Cox regression and least absolute shrinkage and selection operator (LASSO) Cox regression. A novel four-LMRG signature (PROCA1, CCKBR, CPT2, and FDFT1) was constructed to predict clinical outcomes in CRC patients. The risk signature was shown to be an independent prognostic factor for CRC and was associated with tumour malignancy. Principal components analysis demonstrated that the risk signature could distinguish between low- and high-risk patients. There were significantly differences in abundances of tumor-infiltrating immune cells and mutational landscape between the two risk groups. Patients in the low-risk group were more likely to have higher tumor mutational burden, stem cell characteristics, and higher PD-L1 expression levels. Furthermore, a genomic-clinicopathologic nomogram was established and shown to be a more effective risk stratification tool than any clinical parameter alone. This study demonstrated the prognostic value of LMRG and showed that they may be partially involved in the suppressive immune microenvironment formation.
ISSN:1471-2407
1471-2407
DOI:10.1186/s12885-021-08902-5