NK-cell dysfunction of acute myeloid leukemia in relation to the renin–angiotensin system and neurotransmitter genes

Author:

Turk Seyhan1,Baesmat Ayriana Safari2,Yılmaz Aysegul2,Turk Can2,Malkan Umit Yavuz3,Ucar Gulberk1,Haznedaroğlu Ibrahim Celalettin3

Affiliation:

1. Department of Biochemistry, Faculty of Pharmacy, Hacettepe University , Ankara , 06105 , Turkey

2. Department of Medical Microbiology, Faculty of Medicine, Lokman Hekim University , Ankara , 06105 , Turkey

3. Department of Internal Medicine, Faculty of Science, Hacettepe University , Ankara , 06105 , Turkey

Abstract

AbstractAcute myeloid leukemia (AML) is the most heterogeneous hematological disorder and blast cells need to fight against immune system. Natural killer (NK) cells can elicit fast anti-tumor responses in response to surface receptors of tumor cells. NK-cell activity is often impaired in the disease, and there is a risk of insufficient tumor suppression and progression. The aim of this study is to assess the dysfunction of NK cells in AML patients via focusing on two important pathways. We obtained single-cell RNA-sequencing data from NK cells obtained from healthy donors and AML patients. The data were used to perform a wide variety of approaches, including DESeq2 (version 3.9), limma (version 3.26.8) power differential expression analyses, hierarchical clustering, gene set enrichment, and pathway analysis. ATP6AP2, LNPEP, PREP, IGF2R, CTSA, and THOP1 genes were found to be related to the renin–angiotensin system (RAS) family, while DPP3, GLRA3, CRCP, CHRNA5, CHRNE, and CHRNB1 genes were associated with the neurotransmitter pathways. The determined genes are expressed within different patterns in the AML and healthy groups. The relevant molecular pathways and clusters of genes were identified, as well. The cross-talks of NK-cell dysfunction in relation to the RAS and neurotransmitters seem to be important in the genesis of AML.

Publisher

Walter de Gruyter GmbH

Subject

General Medicine

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