Background: Glutathione peroxidases (GPXs) are an enzyme family with peroxidase activity. Abnormal GPX expression is associated with carcinogenesis. However, the potential role of the GPX gene family in acute myeloid leukemia (AML) remains to be comprehensively examined. Methods:We analyzed GPX mRNA expression levels and determined the correlation between gene expression and the prognostic value via multiple universally acknowledged databases including the Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), PROGgeneV2, UALCAN, Cancer Cell Line Encyclopedia (CCLE), and The European Bioinformatics Institute (EMBL-EBI) databases. The functional network of differentially expressed GPXs was investigated via the NetworkAnalyst platform.Correlated genes as well as kinase, microRNA (miRNA), and transcription factor (TF) targets were identified using LinkedOmics. Results:We observed that the transcriptional expression levels of GPX-1, -2, -4, -7, and -8 had significant difference between AML patients samples and normal samples, and that AML patients with high expression of GPX-1, -3, -4, and -7 were associated with poorer prognosis of overall survival (OS). Functional enrichment analysis showed that the differentially expressed GPXs were mainly enriched in response to oxidative stress, regulation of immune response, and inflammatory response, along with glutathione metabolism and ferroptosis. Overexpression of correlated genes, PSMB10, VPS13D, NDUFS8, ATP5D, POLR2E, and HADH were linked to adverse OS in AML. Regulatory network analysis indicated that differentially expressed GPXs regulated cell proliferation, cancer progression, apoptosis, and cell cycle signaling via pathways involving cancer-related kinases (such as DAPK1 and SRC), miRNAs (such as miR-202 and miR-181), and TFs (such as SRF and E2F1).Conclusions: Our findings offer novel insights into the differential expression and prognostic potential of the GPX family in AML, and lay a foundation for subsequent research of GPX's role in the carcinogenesis and regulatory network of AML.

Lung cancer is a leading cause of mortality worldwide and despite recent improvements in lung cancer treatments patient mortality remains high. miR-193a-5p serves a crucial role in the initiation and development of cancer; it is necessary to understand the underlying molecular mechanisms of miR-193a-5p in lung cancer, which may enable the development of improved clinical diagnoses and therapies. The present study investigated the diagnostic value of peripheral blood and tissue miR-193a-5p expression using a microarray meta-analysis. Peripheral blood miR-193a-5p was revealed to be upregulated in patients with lung cancer. The pooled area under the curve (AUC) was 0.67, with a sensitivity and specificity of 0.74 and 0.56, respectively. Conversely, the peripheral tissue miR-193a-5p expression in patients with lung cancer was significantly downregulated. The pooled AUC was 0.83, and the sensitivity and specificity were 0.65 and 0.89, respectively. Through bioinformatics analysis, three Kyoto Encyclopedia of Genes and Genomes (KEGG) terms, pathways in cancer, prostate cancer and RIG-I-like receptor signaling pathway, were identified as associated with miR-193a-5p in lung cancer. In addition, in lung cancer, six key miR-193a-5p target genes, receptor tyrosine-protein kinase erbB-2 (ERBB2), nuclear cap-binding protein subunit 2 (NCBP2), collagen α-1(I) chain (COL1A1), roprotein convertase subtilisin/kexin type 9 (PCSK9), casein kinase II subunit α (CSNK2A1) and nucleolar transcription factor 1 (UBTF), were identified, five of which were significantly upregulated (ERBB2, NCBP2, COL1A1, CSNK2A1 and UBTF). The protein expression of ERBB2, NCBP2, COL1A1, CSNK2A1 and UBTF was also upregulated. NCBP2 and CSNK2A1 were negatively correlated with miR-193a-5p. The results demonstrated that miR-193a-5p exhibited opposite expression patterns in peripheral blood and tissue. Upregulated peripheral blood miR-193a-5p and downregulated tissue miR-193a-5p may be promising diagnostic biomarkers in lung cancer. In addition, the KEGG terms pathways in cancer, prostate cancer and RIG-I-like receptor signaling pathway may suggest which pathways serve vital roles in lung cancer by regulating miR-193a-5p. In addition, six genes, ERBB2, COL1A1, PCSK9, UBTF and particularly NCBP2 and CSNK2A1, may be key target genes of miR-193a-5p in lung cancer.

Normal karyotype acute myeloid leukemia (NK‐AML) is a highly heterogeneous malignancy that resides within a complex immune microenvironment, complicating efforts to reveal the interaction between leukemia cells and immune cells. Understanding tumor‐infiltrating T cells is crucial to the advancement of immune therapies and the improvement of the prognosis for NK‐AML patients. We performed single‐cell RNA sequencing on bone marrow cells from 5 NK‐AML (M4/M5) patients and 1 normal donor and paired single‐cell T cell receptor (TCR) sequencing on single T cells. As a result, we identified 8 T cell clusters based on the gene expression characteristics of each subset in NK‐AML and described their developmental trajectories. In NK‐AML patients, specific clusters, such as mucosal‐associated invariant T cells (MAITs), were preferentially enriched and potentially clonally expanded. These transcriptome and TCR data analyses provide valuable insights and rich resources for understanding the immune environment of NK‐AML.