LAPTM4B promotes AML progression through regulating RPS9/STAT3 axis

被引:2
|
作者
Huang, Yongxiu [1 ]
Peng, Meixi
Qin, Huanhuan [4 ]
Li, Yan [3 ]
Pei, Li [2 ]
Liu, Xindong [1 ,5 ]
Zhao, Xueya [3 ]
机构
[1] Chongqing Univ, Sch Med, 83 Shabei St, Chongqing 400044, Peoples R China
[2] Army Med Univ, Third Mil Med Univ, Southwest Hosp, Dept Hematol, 30 Gaotan Yanzheng St, Chongqing 400038, Peoples R China
[3] Chongqing Med Univ, Biol Sci Inst, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China
[4] Zunyi Med Univ, Zunyi 563000, Guizhou, Peoples R China
[5] Army Med Univ, Southwest Hosp, Inst Pathol, Southwest Canc Ctr, Chongqing 400038, Peoples R China
基金
中国国家自然科学基金;
关键词
Acute myeloid leukemia; LAPTM4B; Progression; RPS9; STAT3; GENE POLYMORPHISM; EXPRESSION; CANCER; SUSCEPTIBILITY; RESISTANCE; STAT3; ACTIVATION; INDUCTION;
D O I
10.1016/j.cellsig.2023.110623
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Acute myeloid leukemia (AML) is a heterogeneous disorder with high morbidity and mortality under the existing treatment strategy. Here, we found that lysosome-associated protein transmembrane 4 beta (LAPTM4B) was frequently upregulated in AML, and high LAPTM4B was associated with poor outcome. Moreover, LAPTM4B promoted leukemia progression in vitro and in vivo. Mechanically, LAPTM4B interacted with RPS9, and positively regulated RPS9 protein stability, which enhanced leukemia cell progression via activating STAT3. Our findings indicate for the first time that LAPTM4B contributes to leukemia progression in a RPS9/STAT3-dependent manner, suggesting that LAPTM4B may serve as a promising target for treatment of AML.
引用
收藏
页数:10
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