Conclusion
miR-324-3p can act as a tumor suppressor in NPC cells by the negative regula- tion of GLI3 gene.
Methods
In total, 54 NPC and 35 control tissues were collected. The correlation between miR-324-3p expression and the clinicopathologic characteristics was analyzed. A dual-luciferase reporter gene assay was employed to examine the predicted target gene of miR-324-3p. The miR-324-3p expression level in 5-8F cells was determined with quantitative reverse transcription-polymerase chain reaction following the transfection of miR-324-3p mimics and inhibitors. Cell proliferation and the percentage of apoptosis were measured with MTT and flow cytometry. Cell invasion ability was assessed by Transwell invasion assay.
Objective
This study aimed to determine the expression, clinical significance, and possible biologic function of microRNA-324-3p in nasopharyngeal carcinoma (NPC) tissues.
Results
Our results showed that miR-324-3p was downregulated in the NPC tissues. The expression level of miR-324-3p in poorly differentiated NPC was significantly reduced in comparison with that in well/moderately differentiated NPC. The expression level in clinical stages III/IV was lower than that in clinical stages I/II. Moreover, the expression level of miR-324-3p was significantly lower in NPC patients with lymph node metastasis than that in NPC patients without lymph node metastasis. NPC patients with higher levels of miR-324-3p expression also demonstrated a longer survival time. Predictions from bioinformatics indicated the Hedgehog pathway transcription gene GLI3 as the target gene of miR-324-3p, and the dual- luciferase reporter assay showed that miR-324-3p is directly combined with the 3'-untranslated region of GLI3. The overexpression of miR-324-3p suppressed cell proliferation and invasion, and it enhanced apoptosis in 5-8F cells.