Enhanced MCM5 Level Predicts Bad Prognosis in Acute Myeloid Leukemia

被引:0
作者
Wang, Shuming [1 ]
Wu, Weiqin [2 ]
Han, Xiang [2 ]
机构
[1] Nanjing Med Univ, Dept Pediat Gen Surg, Affiliated Huaian 1 Peoples Hosp, Huaian, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Emergency, Affiliated Huaian 1 Peoples Hosp, Huaian, Jiangsu, Peoples R China
关键词
DNA replication; MCM5; Acute myeloid leukemia; Prognostic marker; Prognosis; EXPRESSION; CANCER; PROGRESSION; GROWTH;
D O I
10.1007/s12033-022-00623-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Acute myeloid leukemia (AML) is a fatal heterogeneous hematologic malignancy. There is an urgent need to identify potential biomarkers to better classify sufferers with bad outcomes that might need more advanced treatment. The objective of this study was to investigate prognostic indicators that predict the outcome of sufferers with AML. The datasets of AML sufferers including mRNA sequencing data and clinical information were acquired from GEO datasets (GSE38865) and TCGA datasets. Kaplan-Meier curves and Cox regression analysis to screen genes correlated to survival. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses biological process analysis were utilized in verifying the function of various genes. Sufferers with elevated MCM5 level exhibited a worse prognosis, according to the survival analysis. It was indicated through multivariate and univariate analysis that MCM5 level was an independent adverse prognostic element for over survival in AML sufferers based on GEO and TCGA datasets. Meanwhile, MCM5 level in AML samples was higher than in normal samples. Additionally, it was indicated through PPI network and functional enrichment analyses that through accelerating cell cycle and DNA replication, MCM5 promoted AML progression. In conclusions, MCM5 level was an independent poor prognostic element in AML sufferers based on GEO and TCGA datasets. This is the first time that MCM5 is reported to be a biomarker of poor prognosis in AML.
引用
收藏
页码:1242 / 1252
页数:11
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