miR-497 and miR-34a retard lung cancer growth by co-inhibiting cyclin E1 (CCNE1)
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Zhiyuan Han1, Yanbin Zhang2, Qiaoyuan Yang1, Binbin Liu1, Jianjun Wu1, Yajie Zhang3, Chengfeng Yang4 and Yiguo Jiang1
1 State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou, P.R. China
2 Department of Pulmonary Tuberculosis, Guangzhou Chest Hospital, Guangzhou, P.R. China
3 Department of Pathology, Guangzhou Medical University, Guangzhou, P.R. China
4 Department of Physiology and Center for Integrative Toxicology, Michigan State University, East Lansing, MI, USA
Yiguo Jiang, email:
Keywords: CCNE1, lung cancer, miR-34a, miR-497
Received: January 05, 2015 Accepted: March 02, 2015 Published: March 29, 2015
Cyclin E1, encoded by the CCNE1 gene, promotes G1/S transition, chromosome instability, and oncogenesis. Here, we show that miR-497 and miR-34a target the 3′-UTR of CCNE1. miR-497 and miR-34a are downregulated in cancer cells and their ectopic expression inhibited cell proliferation and colony formation in vitro, and inhibited tumor growth in a xenograft model. The effect of simultaneous overexpression of miR-497 and miR-34a on the inhibition of cell proliferation, colony formation, and tumor growth, and the downregulation of cyclin E1 was stronger than the effect of each miRNA alone. The synergistic actions of miR-497 and miR-34a partly correlated with cyclin E1 levels. When cells stably expressing CCNE1 were transfected with the Hi-miR-497/34a plasmid, there was no effect on colony formation, compared with that of cells transfected with either Hi-miR497 or Hi-miR34a. These results indicate cyclin E1 is downregulated by both miR-497 and miR-34a, which synergistically retard the growth of human lung cancer cells.
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