Long non-coding RNA FENDRR attenuates the sternness of non-small cell lung cancer cells via decreasing multidrug resistance gene 1 (MDR1) expression through competitively binding with RNA binding protein HuR

被引:35
作者
Gong, Fangchao [1 ]
Dong, Dong [2 ]
Zhang, Ting [3 ]
Xu, Weiling [2 ]
机构
[1] Jilin Univ, Hosp 1, Dept Thorac Surg, Changchun 130021, Jilin, Peoples R China
[2] Jilin Univ, Hosp 1, Dept Radiol, Changchun 130021, Jilin, Peoples R China
[3] Jilin Univ, Hosp 1, Dept Abdominal Ultrasound, Changchun 130021, Jilin, Peoples R China
关键词
FENDRR; MDR1; HuR; Cancer stem cells; Non-small cell lung cancer; MESSENGER-RNA; E-CADHERIN; PROGRESSION; INVASION;
D O I
10.1016/j.ejphar.2019.04.022
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The roles of long non-coding RNA (lncRNA) FENDRR in non-small cell lung cancer (NSCLC) cells progression have never been revealed. As cancer stem cells (CSCs) act important roles in tumor progression, here, we focused on FENDRR roles in NSCLC cell stemness. We found that lncRNA FENDRR expression was significantly decreased in lung cancer tissues and cells, especially in NSCLC cells. Then we constructed NSCLC cells with FENDRR stable overexpression and revealed that FENDRR overexpression attenuated the stemness of NSCLC cells, evident by decreased stemness markers expression and capacity of cell spheroid formation. Mechanistically, we found that FENDRR could directly and specifically bind to the 3' untranslated region (3'UTR) of multidrug resistance gene 1 (MDR1), hinder the binding of RNA binding protein HuR to MDR1 3'UTR and thus decrease MDR1 expression. Finally, we demonstrated that FENDRR exerted its effects on NSCLC cell stemness through the HuR/MDR1 axis. Our results suggest that FENDRR attenuates NSCLC cell stemness through inhibiting the HuR/MDR1 axis.
引用
收藏
页码:345 / 352
页数:8
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