MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

Recent studies suggested that microRNA-200 family microRNAs play critical roles in cancer initiation and metastasis. The underlying mechanism remained elusive. In this study, we show that microRNA-200c is upregulated in nasopharyngeal carcinoma cells. Manipulation of microRNA-200c levels affected ce...

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Bibliographic Details
Published in:Tumor biology 2017-05, Vol.39 (5), p.1010428317703655-1010428317703655
Main Authors: Zhang, Zhen-Zhen, Cao, Heng-Chang, Huang, Dong-Li, Wu, Qi, Chen, Xiao-Fan, Wan, Jun, Zhang, Wei
Format: Article
Language:English
Subjects:
Animals
Authorship
Cancer therapies
Carcinoma - genetics
Carcinoma - pathology
Cell growth
Cell migration
Cell Movement - genetics
Cell Proliferation - genetics
Disease
Epithelial-Mesenchymal Transition - genetics
Gene expression
Gene Expression Regulation, Neoplastic - genetics
Humans
Immunoglobulins
Metastases
Metastasis
Mice
MicroRNAs - antagonists & inhibitors
MicroRNAs - genetics
miRNA
Nasopharyngeal Carcinoma
Nasopharyngeal Neoplasms - genetics
Nasopharyngeal Neoplasms - pathology
Neoplasm Invasiveness - genetics
Pathogenesis
PTEN Phosphohydrolase - biosynthesis
PTEN Phosphohydrolase - genetics
PTEN protein
Roles
Throat cancer
Transfection
Tumor cell lines
Tumors
Xenograft Model Antitumor Assays
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Summary:Recent studies suggested that microRNA-200 family microRNAs play critical roles in cancer initiation and metastasis. The underlying mechanism remained elusive. In this study, we show that microRNA-200c is upregulated in nasopharyngeal carcinoma cells. Manipulation of microRNA-200c levels affected cell growth, migration, and invasion in nasopharyngeal carcinoma cell lines. Furthermore, PTEN was identified as a direct target of microRNA-200c. Overexpression of PTEN resulted in similar effects to those of anti-microRNA-200c transfection. In vivo suppression of microRNA-200c level reduced tumor growth in mice. Overall, our data suggest that microRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN.
ISSN:1010-4283
1423-0380
DOI:10.1177/1010428317703655