Background
Papillary thyroid carcinoma (PTC) is the most common thyroid cancer. Recent studies have reported that circular RNAs (circRNAs) play essential roles in human cancers, including PTC. However, the roles of circRNA plasmacytoma variant translocation 1 (PVT1) in PTC progression and its potential mechanism remain largely unknown.
Conclusion
CircPVT1 knockdown inhibited PTC progression by sponging miR-126. This may indicate circPVT1 as a novel target for treatment of PTC.
Methods
The expressions of circPVT1 and microRNA-126 (miR-126) were measured in PTC tissues and cells by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis, migration and invasion were detected in PTC cells by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry, Western blot or trans-well assays, respectively. The interaction between circPVT1 and miR-126 was explored by bioinformatics analysis, luciferase activity assay and RNA immunoprecipitation. A mouse xenograft model was established to investigate the role of circPVT1 in PTC progression in vivo.
Results
High expression of circPVT1 was shown in PTC tissues and cells and was associated with poor outcomes of patients. Knockdown of circPVT1 suppressed viability, migration and invasion but induced apoptosis in PTC cells. miR-126 was bound to circPVT1 and reduced in PTC tissues and cells. Moreover, inhibition of miR-126 reversed the regulatory effect of the circPVT1 interference on viability, apoptosis, migration and invasion in PTC cells. Besides, circPVT1 knockdown attenuated tumor growth via up-regulating miR-126 in vivo.