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学科主题: 临床医学
题名:
MicroRNA-211 Expression Promotes Colorectal Cancer Cell Growth In Vitro and In Vivo by Targeting Tumor Suppressor CHD5
作者: Cai, Chunxiao1,2; Ashktorab, Hassan3,4; Pang, Xiaowu1; Zhao, Yuan2; Sha, Wei2; Liu, Yulan1; Gu, Xinbin2,4
刊名: PLOS ONE
发表日期: 2012-01-03
DOI: 10.1371/journal.pone.0029750
卷: 7, 期:1
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Multidisciplinary Sciences
研究领域[WOS]: Science & Technology - Other Topics
关键词[WOS]: CARCINOMA ; HYPERMETHYLATION ; FAMILY ; GENES ; 1P36
英文摘要:

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.

语种: 英语
所属项目编号: CA118770 ; CA102681 ; RCMI 2 G12 RR003048
项目资助者: National Cancer Health ; National Center for Research Resources, USA
WOS记录号: WOS:000301123400100
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/50192
Appears in Collections:北京大学第二临床医学院_消化内科_期刊论文

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作者单位: 1.Peking Univ, Peoples Hosp, Dept Gastroenterol, Beijing 100871, Peoples R China
2.Howard Univ, Dept Oral Pathol, Washington, DC 20059 USA
3.Howard Univ, Dept Med, Washington, DC 20059 USA
4.Howard Univ, Ctr Canc, Washington, DC 20059 USA

Recommended Citation:
Cai, Chunxiao,Ashktorab, Hassan,Pang, Xiaowu,et al. MicroRNA-211 Expression Promotes Colorectal Cancer Cell Growth In Vitro and In Vivo by Targeting Tumor Suppressor CHD5[J]. PLOS ONE,2012,7(1).
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