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Journal of Experimental Hematology ; (6): 1344-1347, 2019.
Artigo em Chinês | WPRIM | ID: wpr-775716

RESUMO

Abstract  Numerous studies have confirmed that abnormal activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway is one of the most common induction mechanisms of T-ALL. In recent years, many literature report that multiple abnormally expressed microRNAs (miRNAs) can participate in the development of T-ALL by regulating the PI3K/AKT signaling pathway. For example, overexpression of miR-19 and miR181a can activate the PI3K/AKT signaling pathway, which leads to the development of T-ALL and induction of chemotherapy drug resistance, as well as the low expression of miR-26b and miR-29a. Apart from the inhibitors and traditional Chinese medicines that target the PI3K/AKT signaling pathway, regulation of the expression of the corresponding miRNA may also be a potential treatment protocol for T-ALL. The mechanisms of PI3K/AKT signaling pathway involved in the development of T-ALL, the role of miRNAs in the PI3K/AKT signaling pathway and the targeted therapy based on this signaling pathway are summarized briefly in this review.


Assuntos
Humanos , Leucemia de Células T , MicroRNAs , Fosfatidilinositol 3-Quinases , Leucemia-Linfoma Linfoblástico de Células T Precursoras , Proteínas Proto-Oncogênicas c-akt , Transdução de Sinais
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