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miR-184 Inhibits Tumor Invasion, Migration and Metastasis in Nasopharyngeal Carcinoma by Targeting Notch2

Hong-Ming Zhu, Xue-Song Jiang, Hui-Zi Li, Lu-Xi Qian, Ming-Yu Du, Zhi-Wei Lu, Jing Wu, Xiao-Kang Tian, Qian Fei, Xia He, Li Yin
2018 Cellular Physiology and Biochemistry  
Background/Aims: A recent study found that dysregulated microRNA-184 (miR-184) is involved in the proliferation and survival of nasopharyngeal carcinoma (NPC). This study aimed to evaluate the detailed mechanisms of invasion, migration and metastasis of NPC cells. Methods: Quantitative reverse-transcription PCR (qRT-PCR) and Western blot were used to confirm the expression levels of miR-184 and Notch2. NPC cell invasion and migration were subsequently examined using in vitro cell invasion and
more » ... cell invasion and wound-healing assays, respectively. MicroRNA (miRNA) target gene prediction databases and dual-luciferase reporter assay were adopted to validate the target genes of miR-184. Results: MiR-184 was downregulated in the NPC cell lines. The miR-184 inhibitor increased the number of invading NPC cells, whereas miR-184 mimics inhibited the invasive ability of such cells. The protein level of E-cadherin decreased, whereas those of N-cadherin and vimentin increased in the anti-miR-184 group. This result showed that miR-184 inhibited NPC cell invasion and metastasis by regulating EMT progression. MiRNA target gene prediction databases indicated the potential of Notch2 as a direct target gene of miR-184. Such a notion was then validated by results of dual-luciferase reporter assay. Notably, shRNANotch2 restrained the EMT and partially abrogated the inhibitory effects of miR-184 on EMT progression in NPC cells. Conclusion: MiR-184 functions as a tumour-suppressive miRNA targeting Notch2 and inhibits the invasion, migration and metastasis of NPC. Fig3. Inhibition of MiR-184 increases invasion and migration in CNE-1 and CNE-2 cell lines. (A) The effects of miR-184 inhibitor on migration ability of NPC. (B) The invasion capacity of cells was investigated using a Matrigel invasion assay.
doi:10.1159/000493459 pmid:30223264 fatcat:oweesctqnvfjloqomxxpqcbyqi