Abstract：
OBJECTIVE: To investigate the clinical significance, functional role and potential downstream mechanism of USP5 in acute myeloid leukemia (AML).
METHODS: The expression of USP5 in AML and normal tissues and its correlation with patients\' survival were analyzed based on TCGA database. USP5 was knocked down and overexpressed in Jurkat and HL-60 cells using lentivirus. USP5 mRNA and protein expression were detected by RT-qPCR and Western blot, respectively. Cell proliferation and growth were measured by CCK-8 and methylcellulose colony-forming assay. Flow cytometry was used to analyze cell cycle and apoptosis.
RESULTS: USP5 was highly expression in AML compared with normal tissues. Up-regulation of USP5 was negatively correlated with the survival of AML patients. USP5 knockdown and overexpression inhibited and promoted the proliferation and colony growth of AML cells, respectively. Cell cycle arrest and apoptosis were induced in USP5 knockdown Jurkat and HL-60 cells. Furthermore, USP5 knockdown inhibited the phosphrylation of AKT, mTOR and 4EBP1.
CONCLUSIONS: Overexpression of USP5 predicts poor survival of AML patients. Targeting USP5 suppresses AKT/mTOR/4EBP1 signaling and reduces the proliferation and growth of AML cells.
UNASSIGNED: USP5表达水平在急性髓系白血病中的意义及其对AKT/mTOR/4EBP1信号通路的调控作用研究.
UNASSIGNED: 探讨USP5在急性髓系白血病（AML）中的临床意义、功能作用和潜在下游机制。.
UNASSIGNED: 基于TCGA数据库分析USP5 在AML和正常组织中的表达及其与患者生存的相关性。利用慢病毒在Jurkat和HL60细胞中敲低和过表达USP5 ，分别通过RT-qPCR和Western blot检测USP5 mRNA和蛋白的表达。通过CCK-8和甲基纤维素集落形成实验进行细胞增殖和生长检测，流式细胞术分析细胞周期和细胞凋亡。.
UNASSIGNED: 与正常组织相比，USP5 在AML中高表达，USP5 的上调与AML患者的生存呈负相关。敲减和过表达USP5 分别会抑制和促进AML细胞的增殖和集落生长。敲减USP5 的Jurkat和HL-60细胞可导致细胞周期停滞和细胞凋亡，此外，敲除USP5 可以抑制AKT、mTOR和4EBP1的磷酸化。.
UNASSIGNED: 过表达USP5 与AML患者的不良预后相关。靶向调控USP5可抑制AKT/mTOR/4EBP1信号传导，抑制AML细胞的增殖和生长。.
METHODS: The expression of USP5 in AML and normal tissues and its correlation with patients\' survival were analyzed based on TCGA database. USP5 was knocked down and overexpressed in Jurkat and HL-60 cells using lentivirus. USP5 mRNA and protein expression were detected by RT-qPCR and Western blot, respectively. Cell proliferation and growth were measured by CCK-8 and methylcellulose colony-forming assay. Flow cytometry was used to analyze cell cycle and apoptosis.
RESULTS: USP5 was highly expression in AML compared with normal tissues. Up-regulation of USP5 was negatively correlated with the survival of AML patients. USP5 knockdown and overexpression inhibited and promoted the proliferation and colony growth of AML cells, respectively. Cell cycle arrest and apoptosis were induced in USP5 knockdown Jurkat and HL-60 cells. Furthermore, USP5 knockdown inhibited the phosphrylation of AKT, mTOR and 4EBP1.
CONCLUSIONS: Overexpression of USP5 predicts poor survival of AML patients. Targeting USP5 suppresses AKT/mTOR/4EBP1 signaling and reduces the proliferation and growth of AML cells.
UNASSIGNED: USP5表达水平在急性髓系白血病中的意义及其对AKT/mTOR/4EBP1信号通路的调控作用研究.
UNASSIGNED: 探讨USP5在急性髓系白血病（AML）中的临床意义、功能作用和潜在下游机制。.
UNASSIGNED: 基于TCGA数据库分析USP5 在AML和正常组织中的表达及其与患者生存的相关性。利用慢病毒在Jurkat和HL60细胞中敲低和过表达USP5 ，分别通过RT-qPCR和Western blot检测USP5 mRNA和蛋白的表达。通过CCK-8和甲基纤维素集落形成实验进行细胞增殖和生长检测，流式细胞术分析细胞周期和细胞凋亡。.
UNASSIGNED: 与正常组织相比，USP5 在AML中高表达，USP5 的上调与AML患者的生存呈负相关。敲减和过表达USP5 分别会抑制和促进AML细胞的增殖和集落生长。敲减USP5 的Jurkat和HL-60细胞可导致细胞周期停滞和细胞凋亡，此外，敲除USP5 可以抑制AKT、mTOR和4EBP1的磷酸化。.
UNASSIGNED: 过表达USP5 与AML患者的不良预后相关。靶向调控USP5可抑制AKT/mTOR/4EBP1信号传导，抑制AML细胞的增殖和生长。.
摘要：
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