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miR-29c induces cell cycle arrest in esophageal squamous cell carcinoma by modulating cyclin E expression

2011; Oxford University Press; Volume: 32; Issue: 7 Linguagem: Inglês

10.1093/carcin/bgr078

1460-2180

Dapeng Ding, Zhaoli Chen, Xiaohong Zhao, Jiwen Wang, Jian Sun, Zhen Wang, Fengwei Tan, Xiaogang Tan, Baozhong Li, Fang Zhou, Kang Shao, Ning Li, Bin Qiu, Jie He,

RNA Research and Splicing

Cyclin E is reported to be an important cell cycle regulator, and its dysregulation is implicated in tumorigenesis including esophageal squamous cell carcinoma (ESCC). MicroRNAs (miRNAs) regulate gene expression at the posttranscriptional level and play important roles in tumor initiation and progression. However, the regulation of cyclin E by miRNAs is still unclear in ESCC. In the present study, we found that overexpression of miR-29c inhibited cyclin E expression by targeting 3′ untranslated region of cyclin E messenger RNA in ESCC cells. Moreover, overexpression of miR-29c induced cell cycle G1/G0 arrest through suppression of cyclin E expression, without affecting other G1 phase-related proteins level, such as cyclin D1, cyclin D2, cyclin dependent kinase (CDK) 2 and CDK6. Furthermore, we demonstrated that overexpression of miR-29c inhibited proliferation of ESCC cells in vitro and in vivo. In addition, we detected miR-29c expression in 26 pairs of esophageal tumor-in-site-tissues and 60 pairs of ESCC tissues. The result showed that miR-29c level significantly decreased in ESCC tumor tissues and cell lines compared with normal esophageal epithelia. Taken together, our findings indicated that miR-29c was frequently downregulated in ESCC tissues and cells and suppressed tumor growth by inducing cell cycle G1/G0 arrest mainly through modulating cyclin E expression.