Journal Article

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

Da-Peng Ding, Zhao-Li Chen, Xiao-Hong Zhao, Ji-Wen Wang, Jian Sun, Zhen Wang, Feng-Wei Tan, Xiao-Gang Tan, Bao-Zhong Li, Fang Zhou, Kang Shao, Ning Li, Bin Qiu and Jie He

in Carcinogenesis

Volume 32, issue 7, pages 1025-1032
Published in print July 2011 | ISSN: 0143-3334
Published online May 2011 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgr078
miR-29c induces cell cycle arrest in esophageal squamous cell carcinoma by modulating cyclin E expression

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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.

Journal Article.  4951 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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