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Let-7a inhibits proliferation and induces apoptosis by targeting EZH2 in nasopharyngeal carcinoma cells
Author(s) -
Kemin Cai,
Yi Wan,
Guan Sun,
Lei Shi,
Xueli Bao,
Zhimin Wang
Publication year - 2012
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2012.2027
Subject(s) - nasopharyngeal carcinoma , ezh2 , apoptosis , oncogene , cancer research , cell cycle , cell growth , cell , biology , cancer , medicine , gene expression , gene , genetics , radiation therapy
Let-7a is frequently downregulated in various types of human cancer includingnasopharyngeal carcinoma. However, the underlying mechanism of let-7a action innasopharyngeal carcinoma remains elusive. In this study, we show that the enhancerof zeste homolog 2 (EZH2) is a direct target of let-7a in human nasopharyngealcarcinoma cells. The inhibition of EZH2 in vitro by let-7a, EZH2 siRNA, attenuatednasopharyngeal carcinoma cell growth, inhibited cell proliferation and inducedcell apoptosis. In addition, for each biological process we identified ontology-associatedtranscripts that significantly correlate with EZH2 expression. Finally, the expressionof EZH2 significantly abrogated let-7a-mediated cell proliferation and apoptosisin the nasopharyngeal carcinoma cells. Taken together, our results suggest thatlet-7a and EZH2 may be potential therapeutic targets for nasopharyngeal carcinoma.

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