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miR-26a inhibits invasion and metastasis of nasopharyngeal cancer by targeting EZH2
Author(s) -
Yu Li,
Juan Lü,
Bao Zhang,
Xiong Liu,
Lu Wang,
Si-Yang Li,
Xiaohong Peng,
Xia Xu,
Wendong Tian,
Xiangping Li
Publication year - 2013
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2013.1173
Subject(s) - nasopharyngeal carcinoma , oncogene , ectopic expression , cancer research , ezh2 , microrna , metastasis , carcinogenesis , biology , cancer , cell cycle , in vivo , cell , cell culture , medicine , histone , radiation therapy , gene , genetics
Nasopharyngeal carcinoma (NPC) is a highly invasive and metastatic type of cancer that is widely prevalent in Southern China. Studies have shown that several microRNAs (miRNAs) are implicated in NPC metastasis. Our previous studies have demonstrated that miRNA miR-26a inhibits cell growth and tumorigenesis of NPC through the repression of enhancer of zeste homolog 2 (EZH2). However, the role of miR-26a in NPC metastasis remains unknown. In this study, we showed that ectopic expression of miR-26a inhibited the migratory and invasive capacities of NPC cells in vitro . Additionally, we used a murine model to investigate the role of miR-26a in NPC metastasis and results showed that miR-26a overexpression suppresses the metastatic behavior of NPC cells in vivo . Furthermore, the data demonstrated that miR-26a decreased the expression levels of EZH2 in vitro and in vivo , suggesting that the antimetastatic effect of miR-26a in NPC was mediated by regulating EZH2. Therefore, these findings indicate that miR-26a functions as an antimetastatic miRNA in NPC and that its antimetastatic effects are mediated mainly by repressing EZH2 expression.

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