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Gene ; 652: 48-58, 2018 Apr 30.
Article in English | MEDLINE | ID: mdl-29427737

ABSTRACT

Nasopharyngeal carcinoma (NPC) is a head and neck cancer associated with poor prognosis. Many studies have shown that the epithelial-to-mesenchymal transition (EMT) is important in cancer progression, metastasis, and chemotherapy resistance and that microRNAs (miRNAs) play a key role in chemotherapy resistance associated with EMT. The miRNA miR-139-5p is downregulated in many human cancers and is closely related to tumor progression. The aim of this study was to investigate the ability of miR-139-5p to influence the cisplatin resistance, apoptosis, invasion and migration in NPC cells through the regulation of the EMT. We investigated these processes in parental HNE1 and cisplatin-resistant HNE1/DDP cells transfected with miR-139-5p inhibitors and mimics, respectively. Our results suggest that the upregulation of miR-139-5p expression inhibits proliferation, invasion, migration and EMT in human NPC cells. In addition, we found that miR-139-5p expression levels and DDP-induced apoptosis positively correlate in NPC cells. In conclusion, our results demonstrate that miR-139-5p can regulate the migration, invasion and DDP resistance in human NPC by modulating the EMT. The regulation of miR-139-5p levels might be a new approach to reverse EMT and DDP resistance and counteract metastasis and chemotherapy resistance in human NPC.


Subject(s)
Antineoplastic Agents/pharmacology , Cisplatin/pharmacology , Epithelial Cells/drug effects , Epithelial-Mesenchymal Transition/drug effects , Gene Expression Regulation, Neoplastic , MicroRNAs/genetics , Cell Line, Tumor , Cell Movement , Drug Resistance, Neoplasm/genetics , Epithelial Cells/metabolism , Epithelial Cells/pathology , Epithelial-Mesenchymal Transition/genetics , Humans , MicroRNAs/antagonists & inhibitors , MicroRNAs/metabolism , Molecular Mimicry , Nasopharynx/drug effects , Nasopharynx/metabolism , Nasopharynx/pathology , Oligoribonucleotides, Antisense/genetics , Oligoribonucleotides, Antisense/metabolism
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