miR-411 contributes the cell proliferation of lung cancer by targeting FOXO1

被引:47
作者
Zhao, Zhiju [1 ,2 ,3 ,6 ]
Qin, Limei [4 ]
Li, Shu [5 ]
机构
[1] Univ Sci & Technol China, Sch Life Sci, Innovat Ctr Cell Biol, Hefei 230027, Anhui, Peoples R China
[2] Univ Sci & Technol China, Sch Life Sci, CAS Key Lab Innate Immun & Chron Dis, Hefei 230027, Anhui, Peoples R China
[3] Univ Sci & Technol China, Med Ctr, Hefei 230027, Anhui, Peoples R China
[4] Chinese Acad Sci, Ctr Infect & Immun, Guangzhou Inst Biomed & Hlth, Lab Pathogen Biol, Guangzhou 510530, Guangdong, Peoples R China
[5] Wannan Med Coll, Dept Pathophysiol, Wuhu 241002, Anhui, Peoples R China
[6] Univ Sci & Technol China, Sch Life Sci, 443 Huangshan Rd, Hefei 230027, Anhui, Peoples R China
关键词
Lung cancer; Cell proliferation; miR-411; FOXO1; TRANSCRIPTION FACTORS; TUMOR SUPPRESSION; BREAST-CANCER; MICRORNAS; GENE; EXPRESSION; SENSITIVITY; MUTATIONS; PROTEINS; CYCLE;
D O I
10.1007/s13277-015-4425-8
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Lung cancer is the leading cause of cancer deaths worldwide; the study of microRNAs gives new hope for lung cancer treatment. miR-411 has been demonstrated to be an independent prognostic factor for lung adenocarcinoma, but the role and regulatory mechanism are largely unknown. In the present study, we found miR-411 was overexpressed in the lung cancer cells; overexpression of miR-411 promoted anchorage-dependent and anchorage-independent growths of lung cancer, while miR-411 knockdown reduced this effect. Further study showed forkhead box O1 (FOXO1) was a target of miR-411. Overexpression of miR-411 suppressed the expression of FOXO1; the effect of suppression was abrogated when the mutation occurred in the 3'UTR of FOXO1. Knockdown of FOXO1 in cells which miR-411 was inhibited recapitulated the phenotype of miR-411 overexpression. Taken together, our study revealed miR-411 promoted cell proliferation of lung cancer by targeting tumor suppressor gene FOXO1 and miR-411 might be a potential target for lung cancer therapy.
引用
收藏
页码:5551 / 5560
页数:10
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