Background: Acute myeloid leukemia (AML) is a common hematopoietic malignancy and have unsatisfactory prognosis. Our study aimed to identify hub genes in AML and explore potential biomarkers through integrated bioinformatics.Methods: Microarray datasets were analyzed to screen the differentially expressed genes (DEGs).Functional enrichment analysis was performed, and protein-protein interaction (PPI) network was generated by the STRING (11.0) database and Cytoscape (3.7.2) software. Hub genes were screened and verified through GEPIA2 and GEO microarray database. Sensitivity of AML cell lines with high expression of hub genes to the small-molecule drugs were identified using GSCA Lite.Results: A total of 456 DEGs were identified and top 100 genes were screened out, of which six genes (FLT3, PF4, CD163, MRC1, CSF2RB, PPBP) were upregulated in AML and individually had a worse prognosis by the overall survival (OS) analysis. AML cell lines with FLT3-overexpression and CSF2RB-overexpression were sensitive to most small-molecule drugs, while, AML cells with CD163-overexpression were only sensitive to a few drugs. However, sensitivity to Erlotinib was correlated with high expression of PF4 and PPBP.
Nasal-type NK/T-cell lymphoma (nasal-type NKTL) is one of the most lethal cancers for. Our study aimed to identify hub differentially expressed genes (DE-genes) and their upstream microRNAs between nasal-type NK/T-cell lymphoma (NKTL) tumor samples and normal nasal tissues through integrated bioinformatics. The 503 DE-genes and 106 DE-miRNAs were identified between NKTL and human normal nasal samples. GO and KEGG analysis were significantly enriched in meiotic recombination, regulation of syncytium formation by plasma membrane fusion, deubiquitination, enriched in meiotic recombination, regulation of syncytium formation by plasma membrane fusion, and stem cell division. And 11 differential expression hub genes and their upstream microRNAs were identified between nasal-type NKTL and normal nasal samples. In summary, after a series of analyses, we found that 11 hub DE-genes and their upstream DE-miRNAs (CDC27-miR-548c-3p, FREM2-miR-373 * , ARHGAP29-miR-548c-3p, QSER1-miR-548c-3p, CD3EAP-miR-149 * , between nasal-type NKTL and normal nasal samples. They are highly likely to be serve as promising biomarkers in nasal-type NKTL.
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