@Article{096504017X15002869385155,
AUTHOR = {Fei Ji, Delinaer Wuerkenbieke, Yan He, Yan Ding, Rong Du},
TITLE = {Long Noncoding RNA HOTAIR: An Oncogene in Human Cervical Cancer  Interacting With MicroRNA-17-5p},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {3},
PAGES = {353--361},
URL = {http://www.techscience.com/or/v26n3/56648},
ISSN = {1555-3906},
ABSTRACT = {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. Lossof-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. Pearson’s 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 siHOTAIR 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.},
DOI = {10.3727/096504017X15002869385155}
}