Long Noncoding RNA UCA1 Accelerates Nasopharyngeal Carcinoma Cell Progression By Modulating miR-124-3p/ITGB1 Axis

Abstract

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.

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.

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.