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题目:: MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene.
作者:: Liu(Xia),Lv(Xiao-Bin),Wang(Xiao-Pai),Sang(Yi),Xu(Shuangbing),Hu(Kaishun),Wu(Mansi),Liang(Yi),Liu(Pan),Tang(Jianjun),Lu(Wen-Hua),Feng(Qi-Sheng),Chen(Li-Zhen),Qian(Chao-Nan),Bei(Jin-Xin),Kang(Tiebang),Zeng(Yi-Xin)
状态:: 发布时间2012-07-18 , 更新时间 2012-07-18
期刊:: Cell Cycle
摘要:: The microRNA miR-138 is dysregulated in several human cancers, but the underlying mechanism remains largely unknown. Here, we report that miR-138 is commonly underexpressed in nasopharyngeal carcinoma (NPC) specimens and NPC cell lines. The ectopic expression of miR-138 dramatically suppressed cell proliferation and colony formation in vitro and inhibited tumorigenesis in vivo. Moreover, we identified the cyclin D1 (CCND1) gene as a novel direct target of miR-138. In consistent with the knocked-down expression of CCND1, overexpression of miR-138 inhibited cell growth and cell cycle progression in NPC cells. Furthermore, CCND1 was widely upregulated in NPC tumors, and its mRNA levels were inversely correlated with miR-138 expression. Taken together, our findings suggest that miR-138 might be a tumor suppressor in NPC, which is exerted partially by inhibiting CCND1 expression. The identification of functional miR-138 in NPC and its direct link to CCND1 might provide good candidates for developing diagnostic markers and therapeutic applications for NPC.
语言:: eng
DOI:: 10.4161/cc.20898

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