Background
Nasopharyngeal carcinoma (NPC) is a common malignant cancer that is distributed particularly in Southeastern Asia. Previous studies have manifested that long noncoding RNA urothelial carcinoma associated 1 (UCA1) was involved in NPC tumorigenesis and metastasis. However, the biological mechanism of UCA1 for NPC cell progression requires further investigation.
Conclusion
UCA1 acts as an oncogene to promote NPC cell proliferation by up-regulating ITGB1 through suppressing miR-124-3p in vitro and in vivo, providing a potential target for NPC diagnosis and treatment.
Methods
The expression levels of UCA1, miR-124-3p, integrin beta-1 (ITGB1) were detected by qRT-PCR. Protein expression of ITGB1 was determined by Western blot assay. Cell proliferation, migration and invasion were evaluated by CCK8 and transwell assay, respectively. The interaction between miR-124-3p and UCA1 or ITGB1 was determined by luciferase reporter system, RIP and RNA pull-down assay. Mice model was established by subcutaneously injecting SUNE1 cells stably transfected with sh-UCA1 and sh-NC.
Results
The expression of UCA1 was up-regulated in NPC tissues and cells. However, UCA1 knockdown hindered NPC cell growth, migration and invasion. In addition, the interaction between miR-124-3p and UCA1 or ITGB1 was confirmed by luciferase reporter system, RIP and RNA pull-down assay. Besides, miR-124-3p inhibitor abrogated UCA1 silencing-mediated suppression on cell progression in NPC. Moreover, UCA1 accelerated NPC cell progression through modulating ITGB1 via sponging miR-124-3p. In vivo experiments revealed the interference of UCA1-inhibited tumor growth by regulating miR-124-3p/ITGB1 axis.