热空气
基因敲除
癌变
癌基因
癌症研究
长非编码RNA
小RNA
生物
宫颈癌
癌症
转染
下调和上调
细胞培养
基因
细胞周期
遗传学
作者
Fei Ji,Delinaer Wuerkenbieke,Yan He,Yan Ding,Rong Du
出处
期刊:Oncology Research
[Cognizant, LLC]
日期:2018-04-10
卷期号:26 (3): 353-361
被引量:29
标识
DOI:10.3727/096504017x15002869385155
摘要
Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are a class of significant regulators in various tumorigenesis processes. The lncRNA homeobox transcript antisense RNA (HOTAIR) has been reported to act as a functional lncRNA in cervical cancer development. The present study investigated the underlying mechanism of HOTAIR and miR-17-5p in cervical cancer tumorigenesis. The results showed that HOTAIR expression was significantly upregulated in both cervical cancer tissues and cell lines. Loss-of-function experiments showed that HOTAIR knockdown inhibited the proliferation, migration, and invasion of cervical cells. In addition, miR-17-5p expression was downregulated in cervical cancer tissues and cell lines. Pearsons correlation analysis indicated that miR-17-5p expression was negatively correlated to that of HOTAIR. Luciferase reporter assay revealed that miR-17-5p directly targeted HOTAIR 3-UTR. Rescue experiments showed that miR-17-5p knockdown could reverse the tumor-suppressing effect caused by si-HOTAIR transfection. In summary, our results reveal the tumor-promoting role of HOTAIR in cervical cancer via sponging miR-17-5p, providing a novel therapeutic target for future treatment of cervical cancer.
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