MiRNA-1469 promotes lung cancer cells apoptosis through targeting STAT5a

被引:0
|
作者
Xu, Chengshan [1 ]
Zhang, Ling [1 ]
Li, Hengheng [1 ]
Liu, Zhihua [2 ,3 ]
Duan, Lianning [1 ]
Lu, Chengrong [1 ]
机构
[1] PLA, Air Force Gen Hosp, Aviat Med Res Lab, Beijing 100142, Peoples R China
[2] Chinese Acad Med Sci, Canc Inst & Hosp, State Key Lab Mol Oncol, Beijing 100021, Peoples R China
[3] Peking Union Med Coll, Beijing 100021, Peoples R China
来源
AMERICAN JOURNAL OF CANCER RESEARCH | 2015年 / 5卷 / 03期
基金
中国国家自然科学基金;
关键词
MicroRNA; lung cancer; Stat5a; apoptosis; OSTEOSARCOMA CELLS; LEUKEMIA-CELLS; PROLIFERATION; MICRORNAS; SUPPRESSION; EXPRESSION; ETOPOSIDE; INDUCTION; RESISTANT; PATHWAY;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs play key roles in cell growth, differentiation, and apoptosis. In this study, we described the regulation and function of miR-1469 in apoptosis of lung cancer cells (A549 and NCI-H1650). Expression analysis verified that miR-1469 expression significantly increased in apoptotic cells. Overexpression of miR-1469 in lung cancer cells increased cell apoptosis induced by etoposide. Additionally, we identified that Stat5a is a downstream target of miR-1469, which can bind directly to the 3'-untranslated region of the Stat5a, subsequently reducing both the mRNA and protein levels of Stat5a. Finally, co-expression of miR-1469 and Stat5a in A549 and NCI-H1650 cells partially abrogated the effect of miR-1469 on cell apoptosis. Our results show that miR-1469 functions as an apoptosis enhancer to regulate lung cancer apoptosis through targeting Stat5a and may become a critical therapeutic target in lung cancer.
引用
收藏
页码:1180 / +
页数:11
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