BACKGROUND: Chromodomain-helicase-DNA-binding protein 5 (CHD5) is a newly 
identified tumor suppressor that is frequently downregulated in a variety of 
human cancers. Our previous work revealed that the low expression of CHD5 in 
colorectal cancer is correlated with CHD5 promoter CpG island hypermethylation. 
In this study, we investigated the effect of microRNA-211 (miR-211)-regulated 
CHD5 expression on colorectal tumorigenesis.
METHODOLOGY/PRINCIPAL FINDINGS: miR-211 was predicted to target CHD5 by 
TargetScan software analysis. A stably expressing exogenous miR-211 colorectal 
cancer cell line (HCT-116(miR-211)) was generated using lentiviral transduction 
and used as a model for in vitro and in vivo studies. The expression level of 
miR-211 in HCT-116(miR-211) cells was upregulated by 16-fold compared to vector 
control cells (HCT-116(vector)). Exogenous miR-211 directly binds to the 
3'-untranslated region (3'-UTR) of CHD5 mRNA, resulting in a 50% decrease in 
CHD5 protein level in HCT-116(miR-211) cells. The levels of cell proliferation, 
tumor growth, and cell migration of HCT-116(miR-211) cells were significantly 
higher than HCT-116(vector) cells under both in vitro and in vivo conditions, as 
determined using the methods of MTT, colony formation, flow cytometry, scratch 
assay, and tumor xenografts, respectively. In addition, we found that enforced 
expression of miR-211 in HCT-116 cells was able to alter p53 pathway-associated 
regulatory proteins, such as MDM2, Bcl-2, Bcl-xL, and Bax.
CONCLUSION/SIGNIFICANCE: Our results demonstrate that CHD5 is a direct target of 
miR-211 regulation. Enforced expression of miR-211 promotes tumor cell growth at 
least in part by downregulating the expression level of the CHD5 tumor 
suppressor. Our results provide a better understanding of the association of 
between miR-211-regulated CHD5 expression and CHD5 function in colorectal 
tumorigenesis.