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miR‐539 induces cell cycle arrest in nasopharyngeal carcinoma by targeting cyclin‐dependent kinase 4
Author(s) -
Lv Lingyan,
Wang Yuzhi,
Zhang Qian,
Zang Hongrui,
Wang Xingjie
Publication year - 2015
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3152
Subject(s) - nasopharyngeal carcinoma , cancer research , cell growth , microrna , biology , cell cycle checkpoint , cell cycle , kinase , viability assay , cyclin d1 , cell , medicine , microbiology and biotechnology , gene , radiation therapy , biochemistry , genetics
Abstract Dysregulation of microRNAs has been demonstrated to contribute to malignant progression of cancers, including nasopharyngeal carcinoma (NPC). miR‐539 was previously reported to be significantly downregulated in osteosarcoma. However, the potential role and mechanism of action of miR‐539 in the initiation and progression of NPC remain largely unknown. Quantitative reverse transcription (RT)‐PCR demonstrated that miR‐539 was significantly downregulated in NPC tumour tissues compared with nontumour tissues. The cell viability, colony formation assay and tumourigenicity assays in nude mice showed that miR‐539 could inhibit NPC cell growth in vitro and in vivo . The cyclin‐dependent kinase 4 (CDK4) was verified as a miR‐539 target gene using dual‐luciferase reporter assays, quantitative RT‐PCR and Western blotting and was involved in miR‐539‐regulated NPC cell growth. These results indicated that miR‐539 plays an important role in the initiation and progression of NPC by targeting CDK4 and the miR‐539/CDK4 pathway may contribute to the development of novel therapeutic strategies for NPC in the future. Copyright © 2015 John Wiley & Sons, Ltd.