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

This is the authors' abstract. We don't add key points for this paper.

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.