MiRNA-329 targeting E2F1 inhibits cell proliferation in glioma cells

Journal of Translational Medicine

Ruxiang Xu⁴  Zhiliang Liu⁴  Benfu He³  Li Tan²  Bingxiang Xiao¹ 

[1] The neurosurgery Department, Wuhan General Hospital, Guangzhou Command, PLA, Wu han 430070, P. R. China;Center of Oncology and Hematology, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510230, P. R. China;Oncology Department, PLA 421 Hospital, Guangzhou 510318, P. R. China;The neurosurgery Department, General Hospital of Beijing Military Command of People's Liberation Army (PLA), Bei jing 100700, P. R. China

关键词: Cell proliferation;    MiR-329;    E2F1;    Glioma;   

Others  :  827159
DOI  :  10.1186/1479-5876-11-172

 received in 2013-01-03, accepted in 2013-07-08,  发布年份 2013

【 摘 要 】

Background

MicroRNAs have recently emerged as key regulators of cancers, miR-329 located on 14q32.31 is one of down-regulated miRNAs in glioma, but the function and molecular mechanisms of miR-329 in determining the malignant phenotype of human glioma are elusive. This study therefore was conducted to investigate the role of miR-329 in biological behaviors of human glioma LN18 and T98G cell lines and its molecular mechanisms.

Methods

Nine patients with GBM were analyzed for the expression of miR-329 by quantitative RT–PCR. MiR-329 overexpression was established by transfecting miR-329 precursor into LN18 and T98G cells, and its effects on cell proliferation were studied using MTT assay, anchorage-independent growth ability assay, colony formation assays, Bromodeoxyuridine labeling and immunofluorescence.

The effects of miR-329 on cell cycle were studied by flow cytometry. The target of miR-329 was determined by luciferase assays. The regulation of miR-329 on Akt pathway was determined by western blot.

Results

The E2F1 was identified as the target of miR-329. Overexpression of miR-329 blocked G1/S transition in LN18 and T98G cell lines, dramatically suppressed cell proliferation and the ability of colony formation. MiR-329 significantly decreased the phosphorylation levels of intracellular kinases Akt and expression of cyclin D1, but the expression of p21 was upregulated, cell growth was suppressed by inhibiting E2F1-mediated Akt pathway.

Conclusions

MiR-329 may inhibit cell proliferation in human glioma cells through regulating E2F1-mediated suppression of Akt pathway.

【 授权许可】

   
2013 Xiao et al.; licensee BioMed Central Ltd.

【 图 表 】

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