@Article{096504018X15166199939341,
AUTHOR = {Feng Shuai, Bo Wang, Shuxiao Dong},
TITLE = {miR-522-3p Promotes Tumorigenesis in Human Colorectal Cancer  via Targeting Bloom Syndrome Protein},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {7},
PAGES = {1113--1121},
URL = {http://www.techscience.com/or/v26n7/56726},
ISSN = {1555-3906},
ABSTRACT = {miR-522-3p is known to degrade bloom syndrome protein (BLM) and enhance expression of other proto-oncogenes, leading to tumorigenesis. This study aimed to investigate the molecular mechanisms of miR-522-3p 
in human colorectal cancer (CRC) cells. Expressions of miR-522-3p in CRC and adjacent tissues, as well as 
in normal human colon epithelial cell line (FHC) and five CRC cell lines, were detected. Human CRC cell 
lines, HCT-116 and HT29, were transfected with miR-522-3p mimic, inhibitor, or scrambled controls. Then 
cell viability, apoptosis, cell cycle progression, and the expressions of c-myc, cyclin E, CDK2, and BLM were 
assessed. It was found that miR-522-3p was highly expressed in CRC tissues when compared to adjacent nontumor tissues and was highly expressed in CRC cell lines when compared to FHC cells. miR-522-3p overexpression promoted cell viability, reduced apoptotic cell rate, arrested more cells in the S phase, and upregulated 
c-myc, cyclin E, and CDK2 expression. BLM was a target gene of miR-522-3p, and miR-522-3p suppression 
did not exert antiproliferative and proapoptotic activities when BLM was silenced. These findings demonstrate 
that miR-522-3p upregulation negatively regulates the expression of BLM, with upregulation of c-myc, CDK2, 
and cyclin E, and thereby promoting the proliferation of human CRC cells.},
DOI = {10.3727/096504018X15166199939341}
}