【摘要】 有大量研究证实,磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)信号通路的异常激活是T-ALL最常见的诱发机制之一。近年来的文献报道,多种异常表达的微小RNA(miRNA)可通过调节PI3K/AKT信号通路参与T-ALL的发生发展,如miR-19和miR181a的过表达、miR-26b和miR-29a的低表达均可激活PI3K/AKT信号通路,导致T-ALL的发生并诱导其对化疗药物耐药。除靶向PI3K/AKT信号通路的抑制剂和中药外,调节相应miRNA的表达也可能是一种治疗T-ALL的潜在方案。本文对参与T-ALL发生发展的PI3K/AKT信号通路机制、miRNA在PI3K/AKT信号通路中的作用以及基于该信号通路靶向治疗的最新研究进展作一综述。更多还原

【Abstract】 Numerous studies have confirmed that abnormal activation of the phosphatidylinositol 3-kinase(PI3 K)/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 PI3 K/AKT signaling pathway. For example, overexpression of miR-19 and miR181 a can activate the PI3 K/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-26 b and miR-29 a. Apart from the inhibitors and traditional Chinese medicines that target the PI3 K/AKT signaling pathway, regulation of the expression of the corresponding miRNA may also be a potential treatment protocol for T-ALL. The mechanisms of PI3 K/AKT signaling pathway involved in the development of T-ALL, the role of miRNAs in the PI3 K/AKT signaling pathway and the targeted therapy based on this signaling pathway are summarized briefly in this review.更多还原