Long noncoding RNA FER1L4 suppresses cancer cell growth by acting as a competing endogenous RNA and regulating PTEN expression

被引:133
|
作者
Xia, Tian [1 ]
Chen, Shengcan [1 ]
Jiang, Zhen [1 ]
Shao, Yongfu [1 ]
Jiang, Xiaoming [1 ]
Li, Peifei [1 ]
Xiao, Bingxiu [1 ]
Guo, Junming [1 ]
机构
[1] Ningbo Univ, Sch Med, Zhejiang Key Lab Pathophysiol, Dept Biochem & Mol Biol, Ningbo 315211, Zhejiang, Peoples R China
来源
SCIENTIFIC REPORTS | 2015年 / 5卷
基金
中国国家自然科学基金;
关键词
GASTRIC-CANCER; CERNA HYPOTHESIS; MICRORNA-TARGET; EMERGING ROLES; CIRCULAR RNAS; CROSS-TALK; MIRNA; SPONGES; IDENTIFICATION; TRANSCRIPTION;
D O I
10.1038/srep13445
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Aberrantly expressed long noncoding RNAs (lncRNAs) are associated with various cancers. However, the roles of lncRNAs in the pathogenesis of most cancers are unclear. Here, we report that the lncRNA FER1L4 (fer-1-like family member 4, pseudogene) acts as a competing endogenous RNA (ceRNA) to regulate the expression of PTEN (a well-known tumor suppressor gene) by taking up miR-106a-5p in gastric cancer. We observed that FER1L4 was downregulated in gastric cancer and that its level corresponded with that of PTEN mRNA. Both FER1L4 and PTEN mRNA were targets of miR-106a-5p. Further experiments demonstrated that FER1L4 downregulation liberates miR-106a-5p and decreases the abundances of PTEN mRNA and protein. More importantly, FER1L4 downregulation accelerated cell proliferation by promoting the G(0)/G(1) to S phase transition. We conclude that one mechanism by which lncRNAs function in in tumorigenesis is as ceRNAs for tumor suppressor mRNAs.
引用
收藏
页数:9
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