肿瘤细胞耐药严重影响白血病的治疗效果及预后，探索耐药机制并找到逆转耐药的机理是当前研究的目标。本项目以人类慢性髓性白血病耐药细胞株K562/ADM为研究对象，采用分子生物学方法构建过表达或干扰TRIB2的K562/ADM细胞模型，探索TRIB2对K562/ADM细胞耐药相关蛋白、ERK信号通路及miR-33a-5p表达的影响，明确白血病细胞耐药可能存在的机制。该研究预期将揭示，TRIB2参与K562/ADM细胞的耐药过程；敲低TRIB2可以抑制耐药蛋白的表达、激活ERK信号通路、上调miR-33a-5p的表达而逆转K562/ADM细胞耐药性；还将阐明TRIB2能否通过ERK信号通路调节miR-33a-5p的表达。该项目通过探讨TRIB2逆转K562/ADM细胞耐药的机制，阐明TRIB2调控miR-33a-5p的机理，为克服白血病耐药提供理论基础及治疗的新靶点。

Multidrug resistance is a major obstacle to leukemia treatment and prognosis. The present research aims to explore the mechanism of reversing drug-resistance. In our study, TRIB2 overexpression or interference cell models were constructed to investigate whether TRIB2 affects the expression of drug-resistance-related proteins, ERK signaling pathway and miR-33a-5p, then to clarify the possible mechanism of leukemia drug resistance. Our study is expected to reveal TRIB2 will be involved in the drug resistance of K562/ADM cell, knockdown TRIB2 can reverse K562/ADM cell drug-resistance by inhibiting the expression of drug resistance proteins, activating the ERK signaling pathway and up-regulating the expression of miR-33a-5p. We will also clarify whether TRIB2 regulates miR-33a-5p expression through the ERK signaling pathway. This study aims to elucidate the mechanism of TRIB2 knockdown reversing K562/ADM cell drug resistance, and TRIB2 regulating miR-33a-5p expression. The research will provide theoretical basis and a new therapeutic target for overcoming leukemia drug resistance.