@Article{096504016X14562725373833,
AUTHOR = {Huiqing Lv, Zhongmin Zhang, Yaoxia Wang, Chenglin Li, Weihong Gong, Xin Wang},
TITLE = {MicroRNA-92a Promotes Colorectal Cancer Cell Growth and Migration by Inhibiting KLF4},
JOURNAL = {Oncology Research},
VOLUME = {23},
YEAR = {2015},
NUMBER = {6},
PAGES = {283--290},
URL = {http://www.techscience.com/or/v23n6/57540},
ISSN = {1555-3906},
ABSTRACT = {Colorectal cancer (CRC) is the third most common malignancy with high mortality around the world. However, 
the biological mechanism of CRC carcinogenesis is not completely known. In the present study, we determined 
the role of miR-92a in the regulation of CRC cell motility. Expression of miR-92a is aberrantly upregulated 
in human CRC tissues and cultured cells, as shown by RT-PCR analysis. The effects of miR-92a on the proliferation and migration of human CRC SW620 and LoVo cells were measured by CCK-8 and Transwell assay, 
respectively. Results showed that the proliferation and migration capacity of both SW620 and LoVo cells were 
significantly increased by miR-92a mimic transfection but reduced by miR-92a inhibition. Additionally, KLF4 
was identified as a direct target of miR-92a in CRC cells through bioinformatics and luciferase reporter analysis. 
KLF4 overexpression attenuated the effects of miR-92a on the regulation of CRC cell motility. Further studies 
suggested that the cell cycle inhibitor p21 was aberrantly downregulated in CRC cells, whereas this inhibition 
was reversed by miR-92a inhibitor. In conclusion, our data demonstrated that miR-92a may play a positive role 
in the colorectal carcinogenesis by promoting the proliferation and migration of CRC cells through targeting 
KLF4 as well as downstream p21. This could be an alternative therapeutic target for CRC.},
DOI = {10.3727/096504016X14562725373833}
}