Open AccessmiR156a Mimic Represses the Epithelial–Mesenchymal Transition of Human Nasopharyngeal Cancer Cells by Targeting Junctional Adhesion Molecule A
Author(s) -
Yunhong Tian,
Longmei Cai,
Yunming Tian,
Yinuo Tu,
Hai Bo Qiu,
Gaoqiang Xie,
Donglan Huang,
Ronghui Zheng,
Weijun Zhang
Publication year - 2016
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0157686
Subject(s) - epithelial–mesenchymal transition , gene knockdown , microrna , nasopharyngeal carcinoma , metastasis , cancer research , biology , cancer , cancer cell , microbiology and biotechnology , population , cell culture , medicine , gene , genetics , environmental health , radiation therapy
MicroRNAs (miRNAs) have been documented as having an important role in the development of cancer. Broccoli is very popular in large groups of the population and has anticancer properties. Junctional adhesion molecule A (JAMA) is preferentially concentrated at tight junctions and influences cell morphology and migration. Epithelial–mesenchymal transition (EMT) is a developmental program associated with cancer progression and metastasis. In this study we aimed to investigate the role of miRNAs from broccoli in human nasopharyngeal cancer (NPC). We demonstrated that a total of 84 conserved miRNAs and 184 putative novel miRNAs were found in broccoli by sequencing technology. Among these, miR156a was expressed the most. In addition, synthetic miR156a mimic inhibited the EMT of NPC cells in vitro . Furthermore, it was confirmed that JAMA was the target of miR156a mimic as validated by 3’ UTR luciferase reporter assays and western blotting. Knockdown of JAMA was consistent with the effects of miR156a mimic on the EMT of NPC, and the up-regulation of JAMA could partially restore EMT repressed by miR156a mimic. In conclusion, these results indicate that the miR156a mimic inhibits the EMT of NPC cells by targeting the 3’ UTR of JAMA. These miRNA profiles of broccoli provide a fundamental basis for further research. Moreover, the discovery of miR156a may have clinical implications for the treatment of patients with NPC.