Send to

Choose Destination
BMC Cancer. 2019 Jan 24;19(1):104. doi: 10.1186/s12885-018-5225-5.

microRNA-342-3p targets FOXQ1 to suppress the aggressive phenotype of nasopharyngeal carcinoma cells.

Author information

Department of Rhinology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Department of Rhinology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.



microRNA (miR)-342-3p is frequently dysregulated in human cancers. In the present study, we aimed to explore the expression, prognostic significance, and biological relevance of miR-342-3p in nasopharyngeal carcinoma (NPC).


We examined miR-342-3p expression in 79 paired NPC specimens and corresponding normal tissues and analyzed its prognostic impact on overall survival of NPC patients. Gain- and loss-of-function experiments were conducted to determine the biological roles of miR-342-3p.


Compared with matched normal nasopharyngeal tissues, miR-342-3p was significantly downregulated in NPC (P = 0.0038). Low miR-342-3p expression was significantly correlated with reduced overall survival (P = 0.0084). Ectopic expression of miR-342-3p significantly suppressed proliferation, colony formation, and invasion of NPC cells. In contrast, depletion of miR-342-3p facilitated NPC cell proliferation and invasion. In vivo xenograft studies confirmed that overexpression of miR-342-3p restrained the growth of NPC xenograft tumors. Mechanistically, FOXQ1 served as a functional target of miR-342-3p. There was a significantly negative correlation between miR-342-3p and FOXQ1 expression (r = - 0.487, P = 0.004) in NPC specimens. Overexpression of FOXQ1 rescued the inhibitory effects of miR-342-3p on NPC cell growth and invasion.


miR-342-3p downregulation predicts poor prognosis in NPC patients and shows suppressive activity against NPC growth and invasion through repression of FOXQ1. Restoration of miR-342-3p may represent a potential therapeutic strategy for NPC.


FOXQ1; Growth; Invasion; Nasopharyngeal carcinoma; miR-342-3p

Supplemental Content

Full text links

Icon for BioMed Central Icon for PubMed Central
Loading ...
Support Center