NAP1L5 通过调节急性髓性白血病中 PEG10 的表达促进上皮-间质转化。

IF 2.1 4区医学 Q3 HEMATOLOGY

Leukemia research Pub Date : 2024-11-13 DOI:10.1016/j.leukres.2024.107623

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

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引用次数: 0

摘要

急性髓性白血病（AML）是一种严重威胁人类健康的血液恶性肿瘤。研究表明，NAP1L5 在急性髓性白血病患者中表达升高，但具体的分子机制仍不清楚。因此，本研究旨在探讨 NAP1L5 在 AML 中的致病机制。NAP1L5在AML中的表达水平升高，NAP1L5的上调与肿瘤生长和上皮-间质转化有关。此外，PEG10是NAP1L5的下游调控因子，其过度表达会促进肿瘤生长和上皮-间质转化。更重要的是，PEG10的缺失抑制了NAP1L5过表达引起的负面影响。我们的研究结果表明，NAP1L5是治疗急性髓细胞性白血病的一个新的治疗靶点。

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

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.

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来源期刊

Leukemia research 医学-血液学

CiteScore

4.00

自引率

3.70%

发文量

259

审稿时长

1 months

期刊介绍： Leukemia Research an international journal which brings comprehensive and current information to all health care professionals involved in basic and applied clinical research in hematological malignancies. The editors encourage the submission of articles relevant to hematological malignancies. The Journal scope includes reporting studies of cellular and molecular biology, genetics, immunology, epidemiology, clinical evaluation, and therapy of these diseases.