Title |
miR-16 induction after CDK4 knockdown is mediated by c-Myc suppression and inhibits cell growth as well as sensitizes nasopharyngeal carcinoma cells to chemotherapy
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Published in |
Tumor Biology, September 2015
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DOI | 10.1007/s13277-015-3966-1 |
Pubmed ID | |
Authors |
Qingping Jiang, Yajie Zhang, Mengyang Zhao, Qiulian Li, Ruichao Chen, Xiaobing Long, Weiyi Fang, Zhen Liu |
Abstract |
Cyclin-dependent kinase 4 (CDK4) is a member of cyclin-dependent kinase family which regulates G1 to S cell cycle transition. CDK4 activity is increased in many tumor types. Here, we report a negative automodulatory feedback loop between CDK4 and miR-16 that regulates cell cycle progression in nasopharyngeal carcinoma (NPC). By miRNA array and real-time PCR, we identified upregulation of tumor suppressor miR-16a, which inhibited cell cycle progression and sensitized NPC cells to chemotherapy. CDK4 knockdown reduced the expression of c-Myc, the latter of which directly suppresses the miR-16 expression by directly binding to the miR-16 promoter. Moreover, we found that miR-16 upregulation could reduce CDK4 expression by repressing CCND1 and thus forms a feedback loop via the CDK4/c-Myc/miR-16/CCND1 pathway. Finally, miR-16 was negatively correlated with CDK4 expression in NPC biopsies. In summary, our results define a double-negative feedback loop involving CDK4 and miR-16 mediated by c-Myc that modulates NPC cell growth and chemotherapy sensitivity. |
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Members of the public | 1 | 100% |
Mendeley readers
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Readers by professional status | Count | As % |
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Student > Bachelor | 3 | 19% |
Researcher | 2 | 13% |
Student > Postgraduate | 2 | 13% |
Other | 1 | 6% |
Professor | 1 | 6% |
Other | 3 | 19% |
Unknown | 4 | 25% |
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Chemical Engineering | 1 | 6% |
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Nursing and Health Professions | 1 | 6% |
Other | 2 | 13% |
Unknown | 3 | 19% |