Work

NAP1L5 promotes epithelial–mesenchymal transition by regulating PEG10 expression in acute myeloid leukaemia

Year: 2024

Type: article

Abstract: Acute myeloid leukaemia (AML) is a haematological malignancy that poses a serious threat to human health. Studies have shown that the expression of NAP1L5 is elevated in patients with AML; however, the specific molecular mechanism remains unknown. Therefore, in this study, we aimed to investigate the pathogenic mechanisms of NAP1L5 in AML. The expression level of NAP1L5 was increased in AML, and the upregulation of NAP1L5 was related to tumour growth and epithelial–mesenchymal transition. Furthermore, PEG10 is a downstream regulatory factor of NAP1L5, and its overexpression promotes tumour growth and epithelial–mesenchymal transition. More importantly, the loss of PEG10 inhibited the negative effects induced by NAP1L5 overexpression. Our results suggest that NAP1L5 is a novel therapeutic target for AML treatment. • NAP1L5 expression is elevated in acute myeloid leukaemia (AML). • NAP1L5 upregulation promotes AML cell growth and epithelial-mesenchymal transition. • PEG10 acts as a downstream regulator of NAP1L5 in AML. • PEG10 loss mitigates the effects of NAP1L5 overexpression. • NAP1L5 may serve as a novel therapeutic target for AML treatment.

Source: Leukemia Research

DOI: 10.1016/j.leukres.2024.107623

Authors: Huan Wu, Hang Luo, Meng Wang, YuQing Du, Jiajia Li

Institution: First Affiliated Hospital of Bengbu Medical College

Language: English

Topic: Acute Myeloid Leukemia Research

Subfield: Hematology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: hybrid

Estimated APC paid: $4,050