Conclusions
We provided evidence that miR-99a inhibits NPC cell proliferative ability by inhibiting mTOR. The newly identified miR-99a/mTOR axis provides novel insight into the pathogenesis of NPC and represents a potential therapeutic target for NPC.
Methods
MiR-99a expression in nasopharyngeal carcinoma cells was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay was performed for accessing cell proliferative capacity. Dual-Luciferase reporter gene assay was employed to verify the combination between miR-99a and mTOR.
Objective
Nasopharyngeal carcinoma is the most common head and neck tumor in Southern China and Southeast Asia, presenting high rates of local invasion and early distant metastasis. Abnormally expressed miR-99a has been discovered in many tumors, and it is involved in nasopharyngeal carcinoma as well. This study aims to explore the molecular mechanisms of miR-99a and mTOR in regulating nasopharyngeal carcinoma. Patients and
Results
We found that miR-99a was downregulated while mTOR was upregulated in nasopharyngeal carcinoma cell lines CNE1 and SUNE1. Low expression of miR-99a or high expression of mTOR predicted poor prognosis of nasopharyngeal carcinoma. MiR-99a overexpression inhibited the proliferation of CNE1 and SUNE1 cells through targeting mTOR. Conclusions: We provided evidence that miR-99a inhibits NPC cell proliferative ability by inhibiting mTOR. The newly identified miR-99a/mTOR axis provides novel insight into the pathogenesis of NPC and represents a potential therapeutic target for NPC.