LINC00665 promotes breast cancer progression through regulation of the miR-379-5p/LIN28B axis

被引:77
作者
Ji, Wei [1 ,2 ,3 ,4 ]
Diao, Yu-Ling [2 ,3 ,4 ,5 ]
Qiu, Yi-Ran [2 ,3 ,4 ,5 ]
Ge, Jie [2 ,3 ,4 ,5 ]
Cao, Xu-Chen [2 ,3 ,4 ,5 ]
Yu, Yue [2 ,3 ,4 ,5 ]
机构
[1] Tianjin Med Univ Canc Inst & Hosp, Natl Clin Res Ctr Canc, Publ Lab, Tianjin 300060, Peoples R China
[2] Key Lab Canc Prevent & Therapy, Tianjin 300060, Peoples R China
[3] Tianjins Clin Res Ctr Canc, Tianjin 300060, Peoples R China
[4] Tianjin Med Univ, Key Lab Breast Canc Prevent & Therapy, Minist Educ, Tianjin 300060, Peoples R China
[5] Tianjin Med Univ Canc Inst & Hosp, Dept Breast Canc 1, Natl Clin Res Ctr Canc, Tianjin 300060, Peoples R China
基金
中国国家自然科学基金;
关键词
RNA; METASTASIS; EXPRESSION;
D O I
10.1038/s41419-019-2213-x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Breast cancer is the most common malignant tumor among women worldwide. Although increasing evidence indicates that long noncoding RNAs (lncRNAs) play critical roles during breast tumorigenesis and progression, the involvement of most lncRNAs in breast cancer remains largely unknown. In the current study, we demonstrated that LINC00665 promotes breast cancer cell proliferation, migration, and invasion. Accumulating evidence indicates that many lncRNAs can function as endogenous miRNA sponges by competitively binding common miRNAs. In this study, we demonstrated that LINC00665 functions as a sponge for miR-379-5p, reducing the ability of miR-379-5p to repress LIN28B. LINC00665 promoted breast cancer progression and induced an epithelial-mesenchymal transition-like phenotype via the upregulation of LIN28B expression. Clinically, LINC00665 expression was increased but miR-379-5p expression was decreased in breast cancer tissues compared with that in normal breast tissues in the TCGA database. Furthermore, the expression of LINC00665 was negatively related with miR-379-5p expression. Collectively, our results reveal the LINC00665-miR-379-5p-LIN28B axis and shed light on breast cancer therapy.
引用
收藏
页数:11
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